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ICU Residents Guide

2014 Edition

Introduction to Learning in the

Intensive Care Unit
Society of Critical Care

Residents Guide
To Learning in the
Intensive Care Unit

The information presented in these guidelines was obtained by the Committee on

Resident Education. The validity of the opinions presented, drug dosages, accuracy
and completeness of contents are not guaranteed by SOCCA.

Copyright 2014 by the Society of Critical Care Anesthesiologists, San Francisco, Callifornia.
All rights reserved. Contents may not be reproduced without prior written permission of the publisher. Fifth Edition.

Society of Critical Care Anesthesiologists 44 Montgomery Street, Suite 1605, San Francisco, CA 94104-4703
Table of Contents

Preface iii Section 6: Gastroenterology & Nutrition 111

Contributors vi 24. Gastrointestinal Hemorrhage 112
25. Nutritional Support 116
Section 1: Introduction to the ICU 1 26. Acute Pancreatitis 121
1. Structure, Stafng, and Safety 2 27. Liver Failure 125
2. Analgesia and Sedation in the ICU 7
3. Neuromuscular Blockade 10 Section 7: Renal and Electrolytes 129
4. Transport of the Critically Ill 14 28. Acute Renal Failure and Renal Protection 130
5. Cardiopulmonary Resuscitation 18 29. Acid-Base Balance 134
6. Ethical Issues in the ICU 25 30. Electrolyte Abnormalities 140
31. Fluid Management in the ICU 147
Section 2: Monitoring 29 32. Renal Replacement Therapy 151
7. Routine Monitoring 30
8. Pulse Wave Monitoring 34 Section 8: Hematology and Transfusion 156
9. Ultrasound 37 33. Thromboembolic Disease 157
10. Point of Care Testing in the ICU 42 34. Coagulopathies in the ICU 161
35. Transfusion Therapy 166
Section 3: Neuro Critical Care 46
11. Neurocritical Care 47 Section 9: Infectious Diseases 173
12. Management of Increased ICP 52 36. Severe Sepsis and Septic Shock 174
13. Delirium 56 37. Infections and Antibiotic Therapy 178
38. Management of the Immunocompromised Patient 186
Section 4: Airway and Pulmonary 60
14. Airway Management 61 Section 10: Miscellaneous Topics 190
15. Tracheostomy Management 67 39. Managing Endocrine Emergencies 191
16. Management of Mechanical Ventilation 71 40. Toxicology and Support of Patients with
17. Weaning from Mechanical Ventilation 77 Drug Overdoses 194
41. Solid Organ Transplantation 200
Section 5: Shock and Cardiac Management 81 42. Trauma Management in the ICU 210
18. Management of Shock 82 43. Burn Management 215
19. Diagnosis and Treatment of Dysrhythmias 87 44. Obstetric Critical Care 219
20. Diagnosis and Treatment of Myocardial Ischemia 91 45. Management of the Critically Ill Geriatric Patient 222
21. Valvular Heart Disease 97
22. Adult Congenital Heart Disease 101 Answers 225
23. Extra-Corporeal Life Support and
Ventricular Assist Devices 106

It is only as we develop others that we permanently succeed.

-Harvey S. Firestone

Welcome to critical care. Whether you are using this review guide for your rst rotation
in critical care or your tenth, we hope that you nd it useful as a supplement to the other
reading materials at your disposal.

The delivery of critical care continues to change rapidly. Therapies that were deemed
benecial in the past (drotrecogin alfa, tight glucose control, etc) are now considered
harmful; it is difcult to keep up-to-date with textbooks alone. Our goal is to provide
concise clinically relevant chapters that are useful for the trainee working in the ICU.
Each chapters relevance is illustrated with a sample case, and the concepts are then
reviewed with self-test multiple choice questions. Further in depth learning can be
obtained with the selected reference list at the end of each chapter.

For those who grew up with digital media, we have also tried to incorporate new tech-
nologies by adding videos, hyperlinks, and interactivity.

Finally, we would like to give our heartfelt gratitude to the many trainees and faculty
mentors across the nation who have contributed to this edition and past editions. Without
their help and expertise, we would have never succeeded. Thank you to the prior editors
as well, for without their vision, we would not be here with the fth edition.

Best wishes to the newcomers. May you enjoy the eld as much as we have.

Elizabeth B Mahanna, MD

David W. Shimabukuro, MDCM

Christine A Doyle, MD

Linda L. Liu, MD

May 2014
Preface to the Fourth Edition Preface to the Third Edition

Many things have changed since the last edition was released. Intensivists have witnessed profound changes in the delivery of critical care medicine in
the last decade. A large number of randomized, prospective clinical trials or before and
Perhaps the most obvious is the name of the society. The society has long had strong after studies have impacted the way we practice critical care. Examples include the use
international connections, and after deliberating, we changed the name of the organiza- of drotrecogin alfa activated for the treatment of severe sepsis and septic shock; low tidal
tion to the Society of Critical Care Anesthesiologists - SOCCA for short. volume ventilation in patients with acute lung injury and the acute respiratory distress
syndrome; implementation of ventilator and catheter bundles to reduce nosocomial
In the short time since the last edition was published, we have seen a variety of practices infections; and the use of alpha-2 agonists for sedation of the critically patient. It was
fall into and then out of favor, drugs be released and then withdrawn, monitoring tech- clear that the Anesthesiology Residents Guide to Learning in the Intensive Care Unit
nologies proliferate and the electronic health record become an overriding concern for all was in need of revision. We and the American Society of Critical Care Anesthesiologists
patient care. Even our options for publication are changing. This is likely to be the last (ASCCA) are pleased to provide this revised guide to supplement the critical care read-
edition that is created as a static electronic document. ing material used by anesthesia residents and fellow.
The third edition has been expanded to include several important topics including Echo-
About half of the authors are new for this edition. Where they have revised older chap- cardiography, Traumatic Brain Injury and Organ Donation and Procurement in the
ters, the original authors are again acknowledged at the end of the chapter. ICU. Similar to the second edition, we have retained the short case presentations and
the self-study questions. The reading lists have been updated.
The majority of the authors who participated in the revision of this edition are new. We
would like to thank the previous authors who were either the original authors or who
Sherif A, M.D. helped revise the second edition. We have acknowledged their contributions at the end
Chicago, Illinois of each chapter. The ASCCA is dedicated to timely revisions of this guide and plans are
already underway on the 4th edition.
Miguel Cobas, M.D.
Miami, Florida Daniel Talmor, M.D.
Stephen O. Heard, M.D.
Christine A. Doyle, M.D.
Campbell, California
Preface to the Second Edition Preface to the First Edition

Since the publication date of the rst edition in 1995, the scope and practice of critical The eld of critical care medicine continues to expand as new technologies are de-
care medicine have continued to change. Examples of new issues encountered during veloped and old technologies are rened. Anesthesiologists have been pioneers in the
this time include controversies over pulmonary artery catheter use and pressures over development of critical care medicine. Changes in the health care environment have led
efcient management of critical care services as managed care demands are realized. Ad- the American Society of Critical Care Anesthesiologists to dene the anesthesiologists as
ditionally, during this time period, academic departments have grappled with conicting the perioperative physician. To achieve this role, anesthesia residents must be competent
demands of resident education and efcient patient care in the new medical marketplace. in critical care medicine. Assessing critically ill patients prior to operative procedures,
A primary mission of the American Society of Critical Care Anesthesiologists is to assist management of intraoperative anesthetic care, treating postoperative pain, and manage-
anesthesiology residency programs to educate the future perioperative physicians, who ment of organ function after a surgical procedure is best done by an anesthesiologist.
are todays anesthesia residents and fellows. The hospitalized patients of today are older
and sicker than ever before, and many will travel to locations in hospital where the pri- The members of the Resident Education Task Force of the American Society of Critical
mary medical caregiver will be an anesthesiologist. With proper skills and training, these Care Anesthesiologists have developed this curriculum guide to help residents achieve
anesthesiologists will be the most appropriate caregivers for these critically ill patients, competence in caring for the critically ill and injured patients. This guide is not meant to
helping maintain complex homeostasis by thorough evaluation and management preced- be an exhaustive curriculum for an intensivist but useful for all residents completing an-
ing, during, and following surgical procedures. esthesiology training. These were developed into outlines of the most important concepts
with a reading list for each. Additionally, self-study questions are included with most
The curriculum of the second edition was modied somewhat from the rst edition sections to allow the resident to evaluate his or her current understanding.
by members of the Resident Education Task Force of the American Society of Critical
Care Anesthesiologists in an attempt to bring up-to-date information to the hands of This guide may also be used by residency program directors to evaluate or improve their
residents who are caring for critically ill and injured patients. To this purpose, several own curriculums. It is not our intention that all aspects of critical care mentioned in the
new sections have been added to the topical outline (e.g., ICU Management, Rational guide be part of the two month critical care rotation required by the American Board of
Use of PA Catheters, Lung Protective Strategies); the bulk of the topic outline remains Anesthesiology. Other experiences, including cardiac anesthesia, consult services, and
as a presentation of the most important concepts of critical care. Short case presentations postoperative recovery room would certainly contribute to mastery of these topics.
have been added to provoke interest and increase relevance. Self-study questions remain
(with annotated answer keys) to allow the resident to evaluate his or her understanding.
Reading lists have also been annotated to emphasize the relevance of most references. Charles G. Durbin, M.D., FCCM

Lucy A. Weston, Ph.D., M.D.


Without the help and support of the members of the Resident Education Task Force, this
endeavor would not be possible. Many special thanks to Doug Coursin, Tom Fuhrman,
Gary Hoormann, and especially, Charlie Durbin, who have provided ofcial (and unof-
cial) technical, editorial, and emotional assistance and trusted this editor with such a
monumental task. Thanks to all contributors, particularly those working on new sections
and/or with tight timelines.

Many thanks to Michelle Smith for her secretarial efforts. She has been my third and
fourth hands.

Anna M. Allred, MD Stephanie Cha, MD

Fellow Resident
Vanderbilt University Medical Center The Johns Hopkins Hospital
Nashville, TN Baltimore, MD
Ruben J. Azocar, MD David P. Ciceri, MD
Associate Professor Associate Professor
Tufts Medical Center Texas A&M Medical School
Boston, MA Temple, TX
Anila Balakrishnan, MD T. Miko Enomoto, MD
Resident Assistant Professor
Oregon Health and Science University Oregon Health and Science University
Portland, OR Portland, OR
Kostantin Balonov, MD Adam S. Evans, MD
Assistant Professor Assistant Professor
Tufts Medical Center Mount Sinai School of Medicine
Boston, MA New York, NY
Mark J. Baskerville, MD Brenda G. Fahy, MD
Assistant Professor Professor
Oregon Health and Science University University of Florida
Portland, OR Gainesville, FL
Edward A. Bittner, MD, PhD Steven M. Frank, MD
Assistant Professor Associate Professor
Massachusetts General Hospital The Johns Hopkins Hospitals
Boston, MA Baltimore, MD
Ansgar Brambrink, MD, PhD Mariya Geube, MD
Professor Fellow
Oregon Health and Science University Massachusetts General Hospital
Portland, OR Boston, MA
Mark Caridi-Scheible, MD Thomas J. Graetz, MD
Fellow Assistant Professor
Emory University Hospital Washington University School of Medicine
Atlanta, GA St. Louis, MO
Michael C. Grant, MD Rebecca Kalman, MD
Resident Fellow
The Johns Hopkins University Harvard Medical School, Massachusetts General Hospital
Baltimore, MD Boston, MA
Matt R. Hallman, MD Jeffrey A. Katz, MD
Assistant Professor Attending Physician
University of Washington, Harborview Medical Center Northshore University
Seattle, WA Evanston, IL
Elizabeth Hankinson, MD Sean Kiley, MD
Resident Assistant Professor
University of Washington University of Florida
Seattle, WA Gainesville, FL
Theresa Hartsell, MD, PhD John Klick, MD
Assistant Professor Assistant Professor
The Johns Hopkins University Case Western Reserve University School of Medicine
Baltimore, MD Cleveland, OH
C. Patrick Henson, DO Matthew D. Koff, MD, MS
Assistant Professor Assistant Professor
Vanderbilt University Geisel School of Medicine, Dartmouth-Hitchcock Medical Center
Nashville, TN Lebanon, NH
Ebony J. Hilton, MD Ryan Laterza, MD
Fellow Resident
Medical University of South Carolina Mount Sinai School of Medicine
Charleston, SC New York, NY
Aaron Joffe, DO Darren Malinoski, MD
Associate Professor Associate Professor
University of Washington/Harborview Medical Center Oregon Health and Science University
Seattle, WA Portland, OR
Daniel W. Johnson, MD Tracy McGrane, MD
Assistant Professor Assistant Professor
University of Nebraska Medical Center Vanderbilt University Medical Center
Omaha, NE Nashville, TN
Aalok Kacha, MD, PhD Judson Mehl, DO
Assistant Professor Fellow
University of Chicago University of Kentucky Chandler Medical Center
Chicago, IL Lexintgon, KY

Katie Menzel, MD Jess Reardon, DO
Resident Resident
Oregon Health and Science University The Johns Hopkins University
Portland, OR Baltimore, MD
Matthias Merkel, MD, PhD John Reich, MD
Associate Professor Assistant Professor
Oregon Health and Science University Tufts Medical Center
Portland, OR Boston, MA
Dawn Nye, DO Deborah Rohner, MD
Assistant Professor Assistant Professor
Oregon Health and Science University University of Kentucky Chandler Medical Center
Portland, OR Lexington, KY
Christopher Paciullo, PharmD Evan Roller, MD
Pharmacist Resident
Emory University Hospital Washington University School of Medicine
Atlanta, GA St Louis, MO
Luke Parr, MD Daniel Rubin, MD
Resident Assistant Professor
University of Washington University of Chicago
Seattle, WA Chicago, IL
Rohit Patel, MD Nahel Saied, MBBCh
Assistant Professor Associate Professor
University of Florida Vanderbilt University
Gainesville, FL Nashville, TN
Ronald Pauldine, MD Monirath Saly, MD
Professor Fellow
University of Washington Oregon Health and Science University
Seattle, WA Portland, OR
Jace Perkerson, MD Peter M. Schulman, MD
Fellow Assistant Professor
Oregon Health and Science University Oregon Health and Science University
Portland, OR Portland, OR
Nicholas Pesa, MD Matthew J. G. Sigakis, MD
Fellow Fellow
Case Western Reserve University School of Medicine Harvard Medical School, Massachusetts General Hospital
Cleveland, OH Boston, MA

Mandeep Singh, MD Sheena M. Weaver, MD
Fellow Assistant Professor
Duke University Medical Center Vanderbilt University Medical Center
Durham, NC Nashville, TN
Jarrett Skirball, MD Brian Wessman, MD
Resident Assistant Professor
Oregon Health and Science University Washington University School of Medicine
Portland, OR St Louis, MO
Gary R. Stier, MD, MBA Peggy White, MD
Associate Professor Assistant Professor
Loma Linda University Medical Center University of Florida
Loma Linda, CA Gainesville, FL
Ilya Treskov, MD Joel Zivot, MD
Resident Assistant Professor
Washington University School of Medicine Emory University Hospital
St Louis, MO Atlanta, GA
Andrea Tsai, MD
University of California, San Francisco
San Francisco, CA
John Turnbull, MD
Assistant Professor
University of California, San Francisco
San Francisco, CA
A. Jason Vaught, MD
University of Florida
Gainesville, FL
Eleanor A. Vega, MD
Oregon Health and Science University
Portland, OR
Peter von Homeyer, MD
Assistant Professor
University of Washington School of Medicine
Seattle, WA

Section 1: Introduction to the ICU


Structure, Staffing & Safety

Analgesia & Sedation

Neuromuscular Blockade


Cardiopulmonary Resuscitation

1. Structure, Staffing, and Safety
Gary R Stier MD MBA

Key Points A 67 year-old man is initially admitted to the hospital ward with a diagnosis
of right lobar pneumonia. He has a history of COPD, diabetes mellitus,
The organization of the ICU can affect patient
chronic kidney disease, and hypertension. Initial treatment consists of
aggressive bronchodilators, uids and antibiotics. During the rst hospital
outcomes night, he develops labored breathing, confusion, and hemodynamic
instability (SBP 85 mm Hg; HR 128/minute), and requires transfer to the
High-intensity ICUs have been shown to have ICU. Initial ICU orders are written by the admitting primary care physician
better outcomes over low-intensity ICUs and include aggressive pulmonary care, increased uids, and dopamine
for blood pressure support. During the evening of the second hospital day,
A multidisciplinary team approach is ideal for he demonstrates worsening respiratory distress, persistent hypotension
critically ill patients despite dopamine at 15 mcg/kg/min, and minimal urine output. A blood
transfusion is ordered for a hemoglobin of 9.8 mg/dL. At the strong urging
A robust quality improvement program is of the nursing staff, an intensivist consultation is requested.
necessary to continually improve patient
satisfaction and outcomes

In the United States, 55,000 adult critically ill patients are cared for each day1, with approximately 200,000
patients dying in ICUs each year. The cost of this care is signicant, reaching $81.7 billion nationwide in
2005.2 A considerable amount of this expense is unnecessary, being related to a lack of care coordination and
a failure to utilize evidence-based best practices. Such care results in prolonged hospital lengths of stay and
excessive resource utilization. Within the ICU environment, the organization and structure of critical care
services has signicant impact upon ultimate performance, the achievement of optimal patient outcomes, and
in the cost of care. The attainment of benchmarked outcomes will soon affect payments to both providers and
hospitals. This chapter will review the basic components of ICU organizationstructure, stafng, and quality
improvementthat form the foundation for best outcomes.

An ICU is a well-dened area of a hospital where patients with acute life-threatening illnesses or injuries
receive continuous specialized medical and nursing care. The ICU structure is important, impacting upon
the quality of care delivered, and includes the physical aspects and architectural design of the ICU, available
equipment (monitors, beds, ventilators, imaging devices), type of ICU practice model, leadership arrange-
ment, and ICU-specic policies and order sets.

The architectural plan of the ICU varies among hospitals, incorporating semi-circular, circular, and rectan-
gular designs. Modern designs focus on creating a healing environment with materials and furnishings that
reduce noise, glare, and stress, and have natural lighting.3 Single patient rooms are 1.1)
superior to multi-patient rooms with regard to patient safety, with 4 to 6 feet of space
provided around the bed perimeter to facilitate in-room procedures and services. The Stafng
specic ICU design impacts upon staff communication, unit noise levels, and patient The ICU staff is comprised of physicians, physician extenders, nurses, and professional
safety. Circular designs, which place patients near the nurses station may enhance pa- support staff. Each provider, working within the team concept, plays a vital role in at-
tient safety by earlier detection of adverse patient events, although noise levels tend to taining the best patient outcomes possible.
be excessive. Optimal designs enhance workow efciency and facilitate effectiveness
of patient care.
Physicians provide the daily care and management of the majority of critically ill pa-
tients. Intensivists are physicians with an additional 1 to 2 years of subspecialty training
The monitoring equipment in the ICU includes: continuous electrocardiogram (ECG), in critical care medicine. Intensivists direct the medical care of patients in most ICUs
pulse oximetry, respiratory rate, temperature, capnography, blood pressure (invasive operating as either closed or hybrid units. On-site ICU intensivist coverage utilizes ei-
and noninvasive), central venous pressure, intracranial pressure, and the EEG. Support
equipment include: emergency airway equipment (including laryngoscopes, endotra- Table 1.1: Common ICU Care Bundles
cheal tubes, and beroptic bronchoscopy equipment), invasive and noninvasive me-
chanical ventilators, ICU beds (including specialty beds), equipment for hemodynamic Bundle Interventions
support (infusion pumps, blood warmers, etc.), temporary pacemakers, supplies and Ventilator Bundle - Elevation of the head of the bed 30-45 degrees
adequate lighting for ICU procedures; positive and negative pressure isolation room(s); - Daily sedation vacations and assessment of
and computer stations for access to laboratory data, radiologic imaging studies, active readiness to extubate
medications, and medical information. - Peptic ulcer disease (PUD) prophylaxis
- Deep venous thrombosis (DVT) prophylaxis
- Daily oral care with chlorhexidine
The ICU is organized into one of three practice models: an open unit (referred to as
low-intensity); a semi-closed (hybrid) unit; and a closed unit. Both the semi-closed
and closed unit models are referred to as high-intensity units. The open unit refers Central Line Bundle - Hand hygiene
to the model where the admitting physician manages all aspects of the patients care. - Maximal barrier precautions
- Chlorhexidine skin antisepsis
The admitting physician may request an intensivist consultation to assist in guiding - Optimal catheter site selection, with avoidance of
management decisions, but is not required to do so. A semi-closed (hybrid) unit refers using the femoral vein for central venous access in
to the model where the admitting physician continues to manage most aspects of the adult patients
patients care, but agrees to a mandatory intensivist consultation with co-management - Daily review of line necessity, with prompt removal
of the more complex medical issues. A closed unit refers to a care model in which an of unnecessary lines
intensivist-directed ICU team manages all aspects of the care of the patient. Studies
have demonstrated reduced cost, fewer medical errors, and better patient outcomes with Severe Sepsis Resuscitation - Measure lactate level
high-intensity ICUs.4 Bundle (to be completed - Obtain blood cultures prior to administration of
within 3 hours)* antibiotics
ICU leadership is composed of an appointed physician medical director and a nurse - Administer broad spectrum antibiotics
- Administer 30 mL/kg crystalloid for hypotension or
manager. The medical director has many duties including: setting the overall vision and lactate 4 mmol/L
strategic direction, overseeing ICU policy and guideline development, educating staff,
and reviewing unit performance and quality outcomes. The nurse manager is a hospital-
appointed position, providing clear lines of authority, responsibility, and accountability Severe Sepsis Resuscitation - Apply vasopressors (for hypotension that does not
within the assigned ICU and for ensuring quality of patient care. The nurse manager is Bundle (to be completed respond to initial uid resuscitation to maintain a
responsible for setting nurse practice standards, education, and for assuring cooperation within 6 hours)* mean arterial pressure (MAP) 65 mm Hg)
- In the event of persistent arterial hypotension
with physicians and other ancillary staff. despite volume resuscitation (septic shock) or initial
lactate 4 mmol/L (36 mg/dL):
ICU-specic policies, utilization of care bundles, and use of diagnosis-specic order - Measure central venous pressure (CVP)
sets are necessary for best outcomes. The daily incorporation of care bundles into man- - Measure central venous oxygen Saturation (ScvO2)
agement plans has been shown to minimize medical errors and adverse events, reduce - Remeasure lactate if initial lactate was elevated
the incidence of nosocomial infections, decrease hospital and ICU length of stay, reduce
the cost of care, and improve patient outcomes.5 A care bundle refers to a limited set of *Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al; Surviving
evidence-based interventions (i.e. 3-5 interventions) that when delivered in aggregate, Sepsis Campaign Guidelines Committee including the Pediatric Subgroup: Surviv-
improves outcomes. Care bundles currently exist for a variety of situations, including ing sepsis campaign: International guidelines for management of severe sepsis and
sepsis management, central line placement, prevention of ventilator-associated pneu- septic shock: 2012. Crit Care Med 2013; 41:580-637
monia, indwelling urinary drainage catheters, and many other clinical situations. (Table
ther a dayshift model (majority of ICUs), with availability during the nighttime hours by
beeper or other communication device, or an in-house 24/7 model (30% of university- Table 1.2: ICU Professional Support Staff
afliated ICUs). The benet of one coverage model over the other has not been conclu- Staff Member Duties
sively demonstrated.6 Optimal daytime patient to intensivist ratios should be no more
than 15:1, although higher ratios can be safely managed during off hours. Above this Respiratory Therapist Evaluation of respiratory equipment needs and setup,
ratio, both the quality of care delivered and job satisfaction decline. management of the patient-ventilator system, airway
care, delivery of bronchodilators, monitor blood gases,
obtain ventilator weaning mechanics and supervise the
A physician extender refers to a nurse practitioner or a physicians assistant. A nurse delivery of protocol-driven respiratory care
practitioner (NP) is an RN who has completed advanced graduate level training. NPs Physical Therapist Evaluation and treatment focused on increasing the pa-
have signicant latitude to practice independently, typically under clinical agreements tients strength and functional training, including passive
termed standardized procedures with a designated physician supervisor. Many states range of motion exercises, massage therapy, stretching
have granted NPs independent practice privileges. A physician assistant (PA) has techniques, hot and cold treatments, breathing exercises,
obtained both a Bachelors degree and a Masters degree in physician assistant studies and specialized exercises tailored to specic problem
from an accredited PA program. PAs are licensed to practice by the state medical board areas
and always work under the direct supervision of a physician. As physician extenders, Occupational Therapist Work with patients who have suffered injuries that will
both NPs and PAs are granted extensive patient care duties including: medical manage- adversely impact their ability to live or work normally;
ment decisions, performing procedures, order writing, and coordination of care. Studies identify treatment goals, including exercises to improve
have shown that physician extenders can provide high quality and cost-effective care motor skill development or use of new equipment.
when working within a collaborative medical care team model.7
Clinical Dietitian Collaborate with the critical care team to identify the
nutritional needs of each critically ill patient, creating
Registered nurses (RN) directly provide, or supervise, all bedside patient care. Criti- nutritional programs tailored to the specic requirements
cal care RNs have specialized training and or experience in taking care of critically of the patient. Nutritional assessment and plans (enteral
ill patients. Typical ICU nurse-to-patient ratios vary from 1:1 to 1:2, based on patient vs. parenteral nutrition) are performed early during the
disease acuity, and are dened by written hospital policies. Full-time nurses generally ICU stay
work 40-hours per week with nurse shift lengths ranging from 8 to 12 hours. Evidence Social Worker Focus is mainly on the psychosocial elements of care, in-
from numerous studies has demonstrated an inverse relationship between the level of cluding facilitating discharge planning of socially complex
ICU nurse stafng and patient mortality, adverse outcomes, resource utilization, and patient situations, transitions of the patient from the
staff turnover rates.8 acute care setting to lower levels of care, dealing with
difcult family situations, hospice placements, nursing
home placements, providing emotional support related to
The ICU Pharmacist has important responsibilities that include: attending ICU rounds, critical illness and crisis intervention, managing barriers
evaluating all drug orders, monitoring drug dosing, alerting the medical staff for po- to safe and timely discharge planning, arranging post-
tential adverse drug interactions, recommending cost effective drug substitutions, and discharge follow-up.
helping develop policies and procedures focused on medication safety within the ICU Case Manager An RN or social worker assigned to coordinate and
workow. The presence of a dedicated ICU pharmacist reduces medical errors and facilitate clinical care, manage resource utilization and re-
improves outcomes. imbursement for ICU services, verify insurance coverage
and address nancial barriers, transition the patient to
Professional support staff - respiratory therapists, physical and occupational therapists, the appropriate level of care when ready, coordinate
discharge planning efforts, and participate in performance
dietitians, social workers, and case managers are a vital part of the ICU team in ef- and outcomes management.
forts to ensure quality care delivery, optimal outcomes, and patient satisfaction. Early
involvement and coordination in patient care plans by the professional support staff ity (AHRQ), National Quality Forum (NQF), the Institute for Healthcare Improvement
members reduces the length of ICU stay while conserving economic resources. The (IHI), and the Leapfrog Group have strongly supported efforts to study and evaluate
specic duties of each professional support staff member are outlined in Table 1.2. EBBP, to reduce medical errors, and to develop safety indicators. The Leapfrog Group,
a quality-focused consortium of large corporations, companies, and health care purchas-
Quality ers, providing health benets to more than 34 million Americans, obtains health care
The Institute of Medicine (IOM) published a landmark paper in 1999 entitled To Err services from hospitals that demonstrate safety, affordability, and quality, including
is Human: Building a Safer Healthcare System. In this paper, it was disclosed that intensivist-directed ICUs.
nearly 100,000 patients die each year as a result of medical errors. In response, health-
care policy has been focused on assuring the consistent delivery of evidence-based best Implementing a quality improvement (QI) and safety culture within the ICU is es-
practices (EBBP) and in measuring outcomes. A number of non-prot organizations, sential for reducing medical errors, controlling practice variation, and for improving
such as The Joint Commission (TJC), the Agency for Healthcare Research and Qual- outcomes.9 The components of a successful QI program include: strong leadership and
vision, choosing attainable ICU-specic QI projects, utilizing standardized QI methods, munication skills in a dynamic learning environment.
staff motivation, teamwork, accurate data collection and reporting, careful evaluation
of results, and adopting effective strategies to change physician and staff behavior. QI Information technology (IT) is essential for evaluating the effectiveness of quality
projects should focus on endeavors that are small, simple, and easy to complete, and improvement efforts and for accurate monitoring of ICU performance. Automatic
should be designed to evaluate a broad variety of parameters that reect unit-specic collection of a comprehensive ICU database assures completeness and reliability of
performance. QI projects begin with baseline data collection, performance of the study data collection, which can be utilized to compare unit outcomes with published quality
intervention with data collection, and review of the data at study completion. A typi- benchmarks. Other benets of modern IT include support for computerized physician
cal QI project process should follow an accepted technique of study, such as the PDSA computer entry (CPOE), promoting the use of evidence-based best practices, ensur-
(plan-do-study-act) method. If the QI project is successful in improving unit perfor- ing better diagnosis capture, providing clinical reminders, inclusion of disease-specic
mance, staff acceptance of future QI efforts is facilitated. order sets, better identication of incorrect medication orders, and clear medical record
Effective communication among staff is necessary for optimal patient outcomes. Mul-
tidisciplinary team roundswhich includes providers, nurses, pharmacists, respiratory The evaluation of ICU quality performance relies upon monitoring quality indicators of
therapists, physical therapists, dietitians, social workers, and case managersprovide performance (Table 1.3) and comparing the results with published benchmarks. In-
a forum for all members of the medical team to come together to discuss patient care dividual ICU performance must be evaluated within the context of the ICU case mix
plans, to problem solve, and to coordinate goals of treatment. Multidisciplinary rounds (patient demographics, acuity of illness, presence of co-morbidities); this is done utiliz-
have been shown to improve efciency, outcome, and cost of care.10 Utilization of ing risk prediction models, such as the Acute Physiology and Chronic Health Evaluation
team-based communication-enhancement techniques, such as the SBAR (Situation, (APACHE) score, Mortality and Probability Model (MPM), and the Simplied Acute
Background, Assessment, Recommendation) method, improves transitions of care Physiology Score (SAPS). These models utilize large databases of patient information
(handoffs) between providers, while simulation training focuses on rening team com- that compare outcomes among similar groups of critically ill patients.
Table 1.3: Common ICU Quality Indicators of Performance
ICU Mortality rate
Length of ICU stay (days) Patients with critical illness have high morbidity and mortality. An ICU with modern
equipment, strong medical and nursing leadership, an intensivist-directed care team,
Duration of mechanical ventilation sufcient ancillary staff support, good communication, and effective IT-driven process
Incidence of unplanned extubations improvement efforts, will ensure the best outcomes for patients.
Incidence of ICU readmissions
Infection rates References
Ventilator-associated pneumonias (VAP)
Central line-associated blood stream infections (CLABSI) 1. Halpern NA, Pastores SM: Critical care medicine in the United States 2000-2005: an
Catheter-associated urinary tract infections (CAUTI) analysis of bed numbers, occupancy rates, payer mix, and costs. Crit Care Med 2010;
Rate of compliance with hand hygeine guideline 2. Critical Care Statistics in the United States. Society of Critical Care Medicine, 2012.
Accessed at: on August 5,
Rate of compliance with care bundles 2013.
Sepsis bundle 3. Thompson DR, Hamilton DK, Cadenhead CD, Swoboda SM, Schwindel SM, Anderson
Central line bundle DC, et al: Guidelines for intensive care unit design. Crit Care Med 2012; 40:1586-600
Ventilator bundle 4. Gajic O, Afessa B: Physician stafng models and patient safety in the ICU. Chest
Urinary catheter bundle 2009; 135:1038-44
5. Resar R, Grifn FA, Haraden C, Nolan TW: Using Care Bundles to Improve Health
Incidence of decubitus ulcers Care Quality. IHI Innovation Series white paper. Cambridge, Massachusetts: Institute for
Healthcare Improvement; 2012
Rate of appropriate peptic ulcer disease prophylaxis 6. Kerlin MP, Small DS, Cooney E, Fuchs BD, Bellini LM, Mikkelsen ME, et al: A ran-
domized trial of nighttime physician stafng in the intensive care unit. N Engl J Med
Rate of appropriate DVT prophylaxis 2013; 368:2201-9.
7. Gershengorn HB, Wunsch H, Wahab R, Leaf DE, Brodie D, Li G, Factor P: Impact of
Medical errors rates nonphysician stafng on outcomes in a medical ICU. Chest 2011; 139:1347-53
Incidence of adverse drug reactions 8. Needleman J, Buerhaus P, Pankratz S, Leibson CL, Stevens SR, Harris M: Nurse staff-
ing and inpatient hospital mortality. N Engl J Med 2011; 364:1037-45
Incidence of suboptimal management of pain 9. Curtis JR, Cook DJ, Wall RJ, Angus DC, Bion J, Kacmarek R, et al: Intensive care
unit quality improvement: A how-to guide for the interdisciplinary team. Crit Care Med
Patient/family satisfaction scores 2006; 34:211-8
10. Kim MM, Barnato AE, Angus DC, Fleisher LA, Kahn JM: The effect of multidisci-
Nurse turnover rate plinary care teams on intensive care unit mortality. Arch Intern Med 2010; 170:369-76

1.1 Which of the following statements regarding a closed ICU model is FALSE?
A. Patient care is shared between the admitting physician and the intensivist-led ICU team
B. Patient care is exclusively directed by the intensivist-led ICU team
C. Studies demonstrate better patient outcomes
D. Studies show that cost of care is less compared with an open ICU model

1.2 Which of the following statements concerning care bundles is FALSE?

A. A care bundle refers to the use of a limited set of evidence-based interventions consis-
tently applied to a specic clinical situation
B. Each care bundle consists of a set of 6-10 interventions
C. Consistent use improves outcomes
D. A care bundle exists for the placement and care of central venous lines

1.3 Which of the following statements regarding an ICU quality improvement program is FALSE?
A. Requires strong leadership and vision
B. Uses standardized quality improvement methods
C. Should focus on larger projects with the greatest patient benet
D. Reduces practice variation while improving outcome

1.4 Individual ICU performance should always be evaluated in the context of the specic ICUs
overall severity of illness (i.e. case mix). All of the following are risk prediction models used to
more accurately estimate patient outcomes EXCEPT?

2. Analgesia and Sedation in the ICU
Stephanie Cha MD and Theresa Hartsell MD PhD

Key Points Case: A 70-year old woman with a history of obesity, prior myocardial
infarction, and chronic back pain status post cervical spine fusion is now
Pain and agitation are commonly under-
admitted to the ICU following a multi-level lumbar posterior spinal fusion.
She remains intubated due to concern for airway edema while in prone
recognized and undertreated among ICU position during surgery. On exam she is hypertensive, tachycardic, and
patients noted to have frequent ventilator dyssynchrony. What is the best approach
to sedate this patient and manage her analgesic needs?
Inadequate treatment of pain or agitation
can have detrimental physiologic as well as
psychological effects.

The routine use of reliable rating systems

improves the recognition of pain and agitation
and allows for goal-directed titration of

Lighter levels of sedation are associated

with improved clinical outcomes. Analgesia
Pain is subjective and can be dened as an unpleasant sensory and emotional experience associated with
Opioids are the first-line therapy for actual or potential tissue damage, or described in terms of such damage1. In ICU patients it can take multiple
forms, and may be categorized as resting pain, acute post-surgical pain, chronic pain including neuropathic
analgesia, but the use of non-narcotic adjuncts injury or cancer, pathologic pain, or procedural pain (e.g. manipulation of traumatic injuries, wound care and
can decrease the incidence of unwanted side dressing changes, invasive procedures, or suctioning of airway secretions). Pain in the ICU is both prevalent
effects. and undertreated, and there are important hemodynamic and psychological consequences associated with
unrelieved pain 2. These include impaired wound healing, increased levels of circulating catecholamines, and
Non-benzodiazepene agents such as the development of chronic pain, post-traumatic stress disorder, and a generally lower health-related quality of
life 2.
dexmedetomidine are emerging as the
preferred sedative agents. Routine monitoring of patient pain levels is recommended. Pain may be self-reported by the visual analog
scale (VAS), or inferred by the patients behavior, assuming intact motor function and the absence of neu-
rologic injury. For patients who are unable to self-report their pain, the Behavioral Pain Scale (BPS) and
Critical Care Pain Observation Tool have been found to be the most valid and reliable assessment methods 2.
These scales score patient pain based on the presence of specic pain-related behaviors, which include facial
expressions, body movements, muscle tension, vocalization and/or ventilator compliance. In addition, while a
patients vital sign trend may suggest the degree or presence of pain, it may be misleading and should not be
used alone in the assessment of pain 2.
of life-sustaining interventions (e.g. central venous catheters or endotracheal tubes).
Principles of pain management in the ICU focus on pre-emptive analgesia, or the use of Indications for sedation include anxiolysis, agitation or delirium, discomfort during
analgesics prior to potentially painful ICU procedures, as well as the use of combination mechanical ventilation or ventilator dyssynchrony, and management of intracranial
therapy. IV opioids are considered to be the rst-line treatment of non-neuropathic pain, hypertension. Common sedatives act primarily through centrally mediated inhibition
and it is important to recognize that all opioids are equally effective when titrated to of neuronal signaling, and include barbiturates, benzodiazepines, NMDA antagonists,
comparable clinical endpoints (Table 2.1) 3. Opioids can be administered by continuous, and alpha-2 agonists, as listed in Table 2.2. Adverse effects are similar across sedative
as-needed, or even patient-controlled dosing. Dosing strategy is inuenced by many classes and may include delirium, sleep disturbance, withdrawal, and increased risk for
factors, such as the patients neurologic status (need for frequent neurologic monitor- infection 2.
ing may favor bolus dosing), hemodynamic lability (continuous infusions are least
likely to exacerbate hypotension), and the presence of renal or hepatic dysfunction. It
is also important to recognize that opioids exhibit many adverse side effects, which may Table 2.2: Sedatives
be particularly difcult to manage in critically ill patients. These include respiratory
depression, CNS depression, nausea and vomiting, constipation, withdrawal with acute Sedative Pharmacology Usage Adverse Effects
discontinuation, miosis, and pruritus 3. Propofol Onset: 1-2 min 5 mcg/kg/min injection site pain, hy-
(GABA-A Elimination t1/2: 3-12h load over 5 potension, myocardial
agonist) (short term use) min followed depression, respiratory
Table 2.1: Opioids Hepatic metabolism, by 5-150mcg/ depression/apnea,
Opioid Pharmacology Use no active metabolites kg/min infusion hyperlipidemia, Propofol
(usually < 50 Infusion Syndrome
Remifentanil Onset: 1-3 min 0.5-15mcg/kg/h mcg/kg/min) (PRIS)
Elimination: t1/2: 3-10 min 1-1.5mcg/kg IV load
Tissue esterase metabolism Benzodiazepines Midazolam Midazolam hypotension, respiratory
(GABA-A Onset 2-5 min 0.01-0.05mg/kg depression, withdrawal
Fentanyl Onset: 1-2 min 0.7-10mcg/kg/h agonists) Elimination t1/2: 3-11h load followed by following abrupt discon-
Elimination: t1/2: 2-4h 0.35-0.50mcg/kg IV push (longer if elderly/ 0.02-0.1mg/kg/h tinuation, propylene glycol
Hepatic metabolism q30-60 minutes cirrhotic) infusion toxicity
Morphine Onset: 5-10 min 2-30 mg/h Hepatic metabolism
Elimination t1/2: 3-4h 2-4mg IV push q1-2h Active metabolites *Propylene glycol toxicity
Hepatic metabolism; active renally cleared may be seen with lorazepam
metabolites renally cleared Lorazepam Lorazepam use, and is characterized
Onset: 15-20 min 0.02-0.04 mg/ by metabolic acidosis with
Hydromorphone Onset: 5-15 min 0.5-3mg/h Elimination t1/2: 8-15h kg load followed elevated osmolar gap and
Elimination t1/2: 2-3h 0.2-0.6 mg IV push q1-2h (longer if elderly/ by 0.01-0.1 mg/ renal dysfunction
Hepatic metabolism cirrhotic) kg/h (<10 mg/h)
Hepatic metabolism, infusion
no active metabolites 0.02-0.06 mg/kg
Pharmacologic adjuncts may limit these unwanted side effects by reducing a patients q2-6h push
opioid requirements. Adjunct classes include non-steroidal anti-inammatory drugs Ketamine Onset: 1 min 0.1-0.5 mg/kg Dissociative halluci-
(NSAIDs) and acetaminophen, which antagonize prostaglandins receptors. NSAIDs are (NMDA An- Duration: 10-15 min IV followed by nations (out of body
renally cleared, and must be used cautiously in patients with GI ulcers and increased tagonist) Hepatic metabolism 0.05-0.4 mg/ experience), emergence
bleeding risk due to their nonselective COX inhibition of prostaglandin and platelet Active metabolites kg/h infusion delirium, increased secretions
synthesis. Similarly, acetaminophen dosing must be modied in patients with liver renally cleared (lacrimation, salivation),
increased myocardial oxygen
insufciency. Other adjuncts include ketamine, anti-epileptics (gabapentin and carba- demand, possible increase
mazepine) for the treatment of neuropathic pain, as well as alpha-2 adrenergic agonists in ICP
(clonidine and dexmedetomidine), tramadol, antidepressants, and topical lidocaine3. In
addition, epidural analgesia is recommended for postoperative pain following abdomi- Dexme- Onset: 5-10 min 1 mcg/kg load xerostomia, bradycardia,
nal aortic aneurysm surgery, and should be considered in the management of patients detomidine Elimination t1/2: over 10 minutes hypotension, transient hy-
who have undergone thoraco-abdominal surgeries or who have traumatic rib fractures (alpha-2 1.8-3.1h followed by pertension following bolus
2. The major disadvantage of epidural analgesia is hypotension due to a sympatholytic- agonist) Hepatic metabolism 0.2-0.7 mcg/
kg/h infusion, for
mediated decrease in systemic vascular resistance. <24 h
0.5-1mg/kg IV
Agitation and Sedation
ICU patients frequently require sedating agents to provide comfort and ensure the safety
The most reliable and valid assessment tools for monitoring the depth and quality of Chest 2009; 135:1075-1086
sedation in adult ICU patients include the Richmond Agitation-Sedation Scale (RASS) 4. Sessler CN, Varney K: Patient-focused sedation and analgesia in the ICU. Chest 2008;
and the Sedation-Agitation Scale (SAS), as shown in Table 2.3 2. Monitoring brain 5. Roberts DJ, Harron B, Hall RI: Sedation for Critically Ill or Injured Adults in the Inten-
function (e.g. Bispectral Index, Auditory Evoked Potentials) has also been proposed, sive Care Unit. Drugs 2012; 72(14):1881-1916
but is not well-substantiated 2. EEG monitoring in ICU patients with elevated intracra-
nial pressure, however, may be useful for goal directed titration of sedatives in order to
minimize cerebral metabolic demand 2.

There has recently been a paradigm shift in sedation management. First, lighter levels of
sedation or daily sedation interruption are recommended over deep, uninterrupted seda-
tion. Exceptions include severe lung injury, severe traumatic brain injury, and hemody-
namic instability associated with myocardial ischemia. Findings of clinical trials suggest
shorter duration of ICU length of stay, shorter duration of mechanical ventilation, and
a reduction in radiologic tests ordered for altered mental status 4. Furthermore, a trend
toward better psychosocial outcomes has been associated with lighter levels of sedation
5. While lighter levels may increase a patients metabolic demand through an increased Questions:
stress response, there is no data to suggest an associated increase in the incidence of
myocardial ischemia2. In addition, an analgesic-based regimen is recommended as 2.1 Which of the following conditions may be improved by the use of ketamine for sedation?
E. Recent traumatic brain injury
sedation may mask pain that is present from reasons listed above. Finally, non-ben- F. Extensive psychiatric history
zodiazepine agents are associated with an improved clinical prole, and are preferred G. Asthma exacerbation
in mechanically ventilated patients. Dexmedetomidine in particular, has emerged as a H. Atrial brillation with poor heart rate control
useful new therapy, as it has been shown to be associated with a shorter duration of me-
chanical ventilation, decreased incidence of delirium, improved cognitive function, and 2.2 Which of the following agents has no analgesic property?
A. Ketamine
B. Midazolam
Table 2.3: Richmond Agitation-Sedation Scale (RASS) C. Remifentanil
vs Sedation Agitation Scale (SAS) D. Ketorolac

RASS SAS 2.3 An 80-year old woman has been sedated with propofol at 50 mcg/kg/min for the past 48
hours while requiring mechanical ventilation. Which of the following is most consistent with the
Agitated +4 Combative 7 Dangerously Agitated development of propofol infusion syndrome?
+3 Very Agitated 6 Very Agitated A. Metabolic alkalosis
+2 Agitated 5 Agitated B. Hypokalemia
+1 Restless C. Immune suppression
D. Renal dysfunction
Calm 0 Alert and Calm 4 Calm and Cooperative
Sedated -1 Drowsy 3 Sedated 2.4 Which of the following is a true statement about dexmedetomidine?
-2 Light Sedation 2 Very Sedated A. It is an NMDA receptor antagonist
-3 Moderate Sedation 1 Unarounsable B. Its administration can precipitate both hypertension and hypotension
C. It is predominantly metabolized by the kidneys
-4 Deep Sedation D. It has no effect on the sleep-wake cycle
-5 Unarousable

decreased inammation as compared to midazolam 5. Compared to midazolam, propofol

was also associated with earlier extubation, but carried a greater incidence of hypoten-
sion requiring pressor support, as well as the risk for Propofol Infusion Syndrome (as
listed in Table 2.2) 5.

1. Pain terms: A list with denitions and notes on usage. Recommended by the IASP
subcommittee on taxonomy. Pain 1979; 6:249
2. Barr J, Fraser GL, Puntillo K, et al: Clinical Practice Guidelines for the Management of
Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit. Crit Care Med
2013; 41:263-306
3. Erstad BL, Puntillo K, Gilbert H, et al: Pain Management Principles in the Critically Ill.
3. Neuromuscular Blockade
Monirath Saly MD and Matthias Merkel MD PhD

Key Points A 36 year-old woman with a history of a difcult airway suffered a ruptured
left middle cerebral artery (MCA) aneurysm and was admitted to the
There is still much debate and controversy
neurocritical care unit with a Fisher 3 subarachnoid hemorrhage and a
Hunt and Hess score of 5. She emergently went to the operating room for
surrounding the use of NMBAs in the ICU. clipping of her aneurysm. Over the ensuing week, she slowly started to
regain neurologic function. She was extubated on POD#7. Unfortunately,
The choice in the use of a neuromuscular 48 hours later after extubation, her neurologic function declined and she
blocking agent in the ICU must be guided by had a witnessed aspiration event resulting in severe hypoxia. A decision
an understanding of the drugs properties was made to intubate her urgently. She was induced with IV propofol and
and a risk-benefit analysis. succinylcholine was used as the NMBA given her history of a difcult airway
and need for a rapid sequence induction. Approximately 15 seconds after
Medications given in the ICU and the induction, while performing the endotracheal intubation, the providers
physiology of the critically ill patient noticed peaked T waves on the monitor that immediately progressed into
can affect the pharmacodynamics and pulseless ventricular tachycardia (VT).
pharmacokinetics of NMBAs.

There are many complications of NMBAs

including DVTs, ICU-acquired weakness, The use of neuromuscular blocking agents (NMBAs) in the ICU is still much debated and its use is con-
awareness, and anaphylaxis. troversial. The decision to treat a patient in the ICU with NMBAs (for reasons other than the placement of
an endotracheal tube or a surgical procedure) is a difcult one that is guided more commonly by individual
practitioner preference than by standards based on evidence-based medicine. According to the 2002 guideline
Hourly monitoring to minimize the dosing published by the Society of Critical Care Medicine (SCCM), NMBAs should be used for an adult patient in
and daily reassessment of the indications for an ICU to manage ventilation, manage increased ICP, treat muscle spasms, and decrease oxygen consumption
NMBAs should be performed. only when all other means have been tried without success.1

NMBAs are usually categorized according to their mechanism of action (depolarizing versus nondepolarizing)
and by their duration of action (short, intermediate, and long-acting). The non-depolarizing agents can be
further subdivided by their structural composition (aminosteroids versus benzylisoquinolinium). (Table 3.1)
Depolarizing agents function by binding to postsynaptic acetylcholine receptors in the neuromuscular junc-
tion (NMJ) and cause a persistent depolarization leading to accid paralysis. Nondepolarizing agents act as
competitive antagonists of postsynaptic nicotinic receptors in the NMJ and block the actions of acetylcholine.
The choice of an NMBA for sustained paralysis in the intensive care unit must be guided by an understanding
of the drugs properties and by a risk-benet analysis.2 The practitioner needs to be familiar with the relevant
pharmacologic features for each NMBA including but not limited to structure, ED95 (the dose necessary to
depress a mechanically evoked twitch response by 95% in controls), usual bolus dose, infusion dose range,
onset time, duration and recovery times, major route of elimination, residual activity of major metabolites,
autonomic interactions, and other major side effects.3
possibility of awareness and its deleterious consequences is also present.5,6
Table 3.1: Neuromuscular blocking agents by mechanism of action and
Hypersensitivity reactions associated with NMBAs are usually IgE related. The am-
Short Intermediate Long monium ion in NMBAs is usually the culprit and may hold cross-reactivity with other
(5-10 min) (20-60 min) (60-100 min) inciting agents. Hence, it may be possible to have an anaphylactic reaction after the
Depolarizing Succinylcholine - - rst exposure to NMBAs.5 Surveys from a large French study suggested that the most
frequent perioperative agent responsible for allergic reactions was NMBAs (more so
Non-depolarizing Mivacurium* Atracurium d-Tubocurarine than latex, colloids, and antibiotics).7
cis-Atracurium Doxacurium
Rocuronium Metocurine
Vecuronium Pancuronium Succinylcholine should be avoided in patients 24 to 72 hours after major burns, trauma,
Pipecuronium devastating strokes, and extensive denervation of their skeletal muscle for fear of life
*no longer available threatening hyperkalemia and cardiac arrest.3 Extra-junctional acetylcholine receptors
adapted from: Greenberg SB & Vender J 5, and Miller RD 3 proliferate in the absence of neural activity. Extrajunctional acetylcholine receptors dif-
fer from postjunctional receptors in composition by a subunit (epsilon subunit replaced
Many drugs interact with the actions of NMBAs. Some drugs such as aminoglycoside by a gamma subunit) that allows the ion channel to remain open for a longer period of
antibiotics and magnesium potentiate their actions and could be involved in the patho- time when activated leading to an increase in extracellular potassium concentration.
physiology of muscle weakness following NMBA use. Others such as phenytoin may This, in turn, leads to life threatening concentrations of potassium that can lead to car-
antagonize the paralytic effect. (Table 3.2) diac arrest, especially in patients with an acidosis (hydrogen-potassium shift).3

In terms of drug selection, no specic recommendation can be given due to a lack of

Table 3.2: Drugs that interact with neuromuscular blocking agents
data. However, cis-atracurium was used in a randomized controlled trial in patients
with severe acute respiratory distress syndrome (ARDS).4 In this randomized trial, Drug Effect
the patients receiving a cis-atracurium infusion for the rst 48 hours had an increased Antibiotics (aminoglycosides, vancomycin, Potentiation
adjusted 90-day survival and a signicant improvement in the PaO2:FiO2 ratio even clindamycin, tetracycline, bacitracin)
after the infusion was stopped. Furthermore, patients in the treatment group had higher
number of ventilator-free days, organ failure-free days, and reduced barotrauma.4 Anticonvulsants (phenytoin, carbamazepine) Resistance
Although cis-atracurium was used in this study, the primary goal was to assess the use Antidysrhythmics (lidocaine, calcium Potentiation
of an NMBA versus no NMBA. The 2002 SCCM guideline for sustained neuromus- channel blockers, quinidine, procainamide)
cular blockade in the adult critically ill patient recommends vecuronium, though these
recommendations are currently being revised.1 Common dosing regimens for available Antihypertensives (trimethaphan, nitro- Potentiation
NMBAs can be reviewed in Table 3.3. glycerine)
Dantrolene Potentiation
The need for an NMBA should be reassessed daily and administration should be Inhaled anesthetics Potentiation
stopped as early as possible. Despite the lack of evidence that monitoring prevents ad-
verse effects, in addition to the lack of a standardized method of monitoring, assessment Furosemide Potentiation
of the depth of neuromuscular blockade in ICU patients is recommended. (1) Monitor- Local anesthetics Potentiation
ing the depth of neuromuscular blockade may allow usage of the lowest NMBA dose
and may minimize adverse events.1 By using Train-of-Four (TOF) monitoring, the rate Magnesium Sulfate Potentiation
of infusion can be adjusted to achieve one or two twitches. The TOF (four 2 Hz electri- Ranitidine Resistance
cal stimulus delivered every 0.5 seconds applied to the ulnar, facial, or posterior tibial
nerve) is based on the concept that acetylcholine is depleted by successive stimulations; Steroids Potentiation
with increasing neuromuscular blockade, there will be fade and less twitches.3,5 How- Theophylline Resistance
ever, the TOF might be difcult to assess in an edematous and/or diaphoretic patient.5
adapted from: Greenberg SB & Vender J , and Murray MJ et al
5 1
A second option is to stop the paralytic on a daily basis (drug holiday) to reassess the
need for continuing the drug and assure rapid recovery from the drug effects.1

The complications of neuromuscular blockade in the ICU can be categorized as short-

term (anaphylaxis, ventilator disconnect, accidental extubation, acute hyperkalemia
with succinylcholine use), mid-term (corneal abrasions/ulcerations, edema, hypostasis, NMBAs are not sedatives; therefore, before initiating neuromuscular blockade, patients
pressure ulcers, venous thrombosis) and long-term (muscle weakness). Additionally, the should receive appropriate sedative and analgesic drugs to avoid awareness and post-

traumatic stress disorder (PTSD). The use of depth of anesthesia monitors to assure a
proper level of sedation while patients are paralyzed seems logical although there is
not enough evidence to support their routine use.5,6 There has been no universally ac- References:
cepted bedside monitor to detect awareness in the ICU; processed electroencephalogram
devices, such as the bispectral index (BIS), have been used successfully and unsuccess- 1. Murray MJ, Cowen J, DeBlock H, Erstad B, Gray AW Jr, Tescher AN, McGee WT,
fully to detect awareness in the ICU.5,6 Prielipp RC, Susla G, Jacobi J, Nasraway SA Jr, Lumb PD; Task Force of the American
College of Critical Care Medicine (ACCM) of the Society of Critical Care Medicine (SCCM),
American Society of Health-System Pharmacists, American College of Chest Physicians:
Although thought to be multifactorial, prolonged skeletal muscle weakness in ICU Clinical practice guidelines for sustained neuromuscular blockade in the adult critically ill
patient. Crit Care Med 2002; 30:142-56.
patients is closely related to the use of NMBAs.8,9 A confusing list of names and
syndromes, including acute quadriplegic myopathy syndrome (AQMS), oppy man 2. Ortega R, Azocar R: Neuromuscular Blocking Agents, Surgical Intensive Care Medi-
syndrome, critical illness polyneuropathy (CIP), critical illness myopathy (CIM), criti- cine. Edited by ODonnell J, Nacul F. Norwood, Kluwer Academic Publishers, 2001, pp
cal illness polyneuromyopathy (CIPNM), acute myopathy of intensive care, rapidly 163-80.
evolving myopathy, acute myopathy with selective lysis of myosin laments, acute 3. Miller RD: Neuromuscular blocking drugs, Basics of Anesthesia, 6th edition. Edited by
steroid myopathy, and prolonged neurogenic weakness have been reported in the litera- Miller RD, Pardo M. Philadelphia, Elsevier-Saunders, 2011, pp 143-61.
ture. 1,5,10 However, the term ICU-acquired weakness has become the more frequently
used catchall phrase for this disease process.5,11 Although the exact mechanisms of 4. Forel JM, Roch A, Marin V, Michelet P, Demory D, Blache JL, Perrin G, Bondgrand P,
Papazian L: Neuromuscular blocking agents decrease inammatory response in patients
this problem are unknown, the common factor seems to be damage to the neuromus- presenting with acute respiratory distress syndrome. Crit Care Med 2006; 34: 2749-57.
cular membrane.11 The use of steroid-based NMBAs (pancuronium, vecuronium)
and/or the concomitant use of steroids have been associated in the development of 5. Greenberg SB, Vender J: The use of neuromuscular blocking agents in the ICU: Where
prolonged muscle weakness.1,12,13,14 However, benzylisoquinolinium-based NMBAs are we now? Crit Care Med 2013; 41:1332-44.
(cis-atracurium, atracurium) have also been reported to produce this phenomenon.1,14 In 6. Arbour R: Impact of bispectral index monitoring on sedation and outcomes in critically
addition, muscle weakness has been associated with the persistent presence of the drug ill adults: a case series. Crit Care Nurs Clin North Am 2006; 18:227-41.
or its metabolites in plasma. Alterations in clearance mechanisms such as hepatic and/or
renal failure can contribute to this problem.15 Unintentional overdose, drug interactions 7. Mertes PM, Laxenaire MC, Alla F; Groupe dEtudes des Ractions anaphylactodes
Peranesthsiques: Anaphylactic and anaphylactoid reactions occurring during anesthesia
(Table 3.2), electrolyte imbalances (hypermagnesemia, hypophosphatemia), acidosis, in France in 1999-2000. Anesthesiology 2003; 99(3):536-45.
hypothermia and underlying muscle disorders (polyneuropathy of critical illness, myas-
thenia gravis) are also involved.10,15 8. Murray MJ, Brull SJ, Bolton CF: Brief review: Nondepolarizing neuromuscular block-
ing drugs and critical illness myopathy. Can J Anaesth 2006; 53:1148-56.

In summary, NMBAs should be used judiciously in the critically ill patient. The effects 9. Friedrich O: Critical illness myopathy: what is happening? Curr Opin Clin Nutr Metab
of these agents on the neuromuscular membrane can lead to severe adverse events. If Care 2006; 9:403-9.
deemed necessary to use, monitoring the depth of the blockade to minimize dosing and 10. Latronico N, Bolton CF: Critical illness polyneuropathy and myopathy: a major cause
constant reassessment of the indications are vital. If prolonged use is needed, drug of muscle weakness and paralysis. Lancet Neurol 2011; 10:931-41.
holidays should probably be performed.
11. Batt J, dos Santos CC, Cameron JI, Herridge MS: Intensive care unit-acquired weak-
ness: clinical phenotypes and molecular mechanisms. Am J Respir Crit Care Med 2013;
This chapter is a revision of the original chapter authored by Naga Pullakhandam, Devanand 187(3):238-46.
Mangar, and Enrico M Camporesi, MD
12. Douglass JA, Tuxen DV, Horne M, Scheinkestel CD, Weinmann M, Czarny D, Bowes

Table 3.3: Pharmacology of neuromuscular blocking agents

ED95 Onset to Maximum Intubating Dose Continuous Infusion Elimination
(mg/kg) Twitch (min) (mg/kg) (mcg/kg/min)
Succinylcholine 0.3-0.5 <1 1 not recommended plasma cholinesterase
Atracurium 02-0.25 3-5 0.4-0.5 4-20 5-10% renal, Hoffman elimination
cis-Atracurium 0.05 2-3 0.1-0.2 1-3 5-10% renal, Hoffman elimination
Rocuronium 0.3 1-2 0.6-1.2 8-12 10-30% renal, < 75% hepatic
Vecuronium 0.05 3-5 0.08-0.1 0.8-1.7 10-50% renal, 35-50% hepatic
Pancuronium 0.05-0.08 3-5 0.05-0.1 0.8-2 45-70% renal, 10-15% hepatic
adapted from: Greenberg SB & Vender J , Miller RD and Murray MJ et al
5 3 1

G: Myopathy in severe asthma. Am Rev Respir Dis 1992; 146(2):517-9.

13. Op de Coul AA, Lambregts PC, Koeman J, van Puyenbroek MJ, Ter Laak HJ, Gabres-
3.1 All of the following drugs potentiate the effects of NMBAs EXCEPT:
Festen AA: Neuromuscular complications in patients given pavulon (pancuronium bro- A. Aminoglycosides
mide) during articial ventilation. Clin Neurol Neurosurg 1985; 87(1):17-22. B. Magnesium
C. Phenytoin
14. Adejumo SWA, Hunter JM: Muscle relaxants in the critically ill. Curr Opin Crit Care D. Quinidine
1999; 5:263-8.

15. Segredo V, Caldwell JE, Matthay MA, Sharma ML, Gruenke LD, Miller RD: Persistent 3.2 Which of the following NMBAs are NOT appropriately paired based on their duration of ac-
paralysis in critically ill patients after long-term administration of vecuronium. N Engl J tion?
Med 1992; 327(8):524-8. A. Cis-atracurium: short
B. Mivacurium: short
C. Rocuronium: intermediate
D. Vecuronium: intermediate

3.3 Complications of using non-depolarizing NMBAs in the ICU may include all of the following
A. Awareness
B. Critical Illness Myopathy
C. Hyperkalemia
D. Venous Thrombosis

3.4 Potential causes of prolonged weakness in the ICU patient after NMBA administration
include all the following EXCEPT:
A. Concomitant use of steroids
B. Drug or drug metabolites accumulation
C. Electrolyte disturbances
D. Propofol interaction with the neuromuscular junction

4. Transport of the Critically Ill
Ronald Pauldine MD

Key Points A 45 year old man is involved in a high speed motor vehicle collision.
He is transported by ambulance to a nearby rural hospital. He becomes
The goal during transport is to maintain the
unstable during initial assessment in the emergency department
requiring intravascular volume resuscitation and endotracheal intubation.
same monitoring and supportive care that the Identied injuries include blunt chest trauma, pelvic fractures and
patient receives in the intensive care unit. extremity fractures. He is stabilized and arrangements are made for
aeromedical transport by helicopter to a regional trauma center for
It is never just another road trip. Movement further management. On arrival to the trauma center he requires a series
of patients is associated with a number of transports within the hospital. These include movement between the
of adverse events and requires careful emergency department and intensive care unit with transport to specialized
consideration of the reasons for transport. areas for diagnostic imaging, angiographic embolization of pelvic
hemorrhage and operative repair of orthopedic injuries.
It is useful to ask, How likely are the results
of this patient transport to change the present
course of treatment?

Transport personnel should be familiar

with transport procedures and equipment. Introduction
Checklists are a useful tool to facilitate safe Movement of critically ill or injured patients is a common event in the delivery of modern healthcare. Patient
transport and improve communication. movement can occur in a number of settings including the prehospital environment, transfer between facilities
and movement within the hospital. Prehospital transport is classied as primary transport and later move-
ment within or between facilities is designated as secondary transport. Reasons for movement include gaining
access to healthcare via emergency medical services, evacuation from disaster areas or hostile or austere
environments, transfers between facilities for increasing complexity of care and movement within a facility
for diagnostic or therapeutic procedures. Modes of transport vary greatly and include the use of mobile beds,
transport litters, ground vehicles, and rotary wing or xed wing aircraft. While the indications, modes, and
sites of transport are variable, the general concepts governing safe and effective movement of critically ill and
injured patients share many of the same principles.

General Considerations for Patient Transport

Transport of any critically ill patient begins with careful consideration of the necessity of transport, assess-
ment of the patients condition, dening command and control for the process, ensuring appropriate commu-
nication between care teams, choosing a mode of transport, preparing the patient, pre-movement checks of all
equipment and verication of necessary supplies. The transport is performed with attention to transfer of care
at the conclusion along with proper documentation. Critical events should be reported in addition to any pro-
cess or quality improvement information. Specialized equipment is employed for patient transport and often
has signicantly different operational characteristics from the equipment used at the bedside in the intensive
care unit (ICU). It is imperative that transport personnel understand the operation, po-
tential limitations and how to troubleshoot the transport equipment they utilize. Ideally, Table 4.1 Sample Transport Checklist
transport equipment will be interoperable with all equipment across a given system. DECISION TO TRANSPORT
This includes issues such as compatible cables, device interfaces and infusion tubing
sets and cartridges. The process of patient transport is well suited for the use of check- Does the expected benet of transport outweigh the risk?
lists to standardize care and avoid errors of omission. A number of checklists have been Staff/Equipment/Vehicles available?
published for use in the transport environment. A sample transport checklist is provided
in Table 4.1. Receiving location prepared?
A signicant body of literature demonstrates that physiologic derangements occur Adequately trained and experienced
during all phases of transport and transport increases the risk for adverse outcomes.
Adverse events may reect deterioration in one or more physiologic variables or critical Detailed handoff to transport team
situations, which require urgent therapeutic intervention. Several studies have reported EQUIPMENT
complications related to gas exchange with manually assisted ventilation. Transport
ventilators are increasingly employed to mitigate this risk that has been particularly as- All equipment operational
sociated with adverse outcome in brain injury. Adverse events reported across all trans- Portable power supply/Batteries charged
port domains are reviewed in Table 4.2. A wide range of factors have been implicated
in contributing to adverse events. These include human factors relating to knowledge, Alarm limits checked and set
judgment and technical performance, process problems such as inadequate communica- Lines and tubes simplied, secured and labeled
tion, insufcient protocols and lack of training, as well as multiple problems with trans-
port equipment. Prehospital and interhospital transport are associated with an increased Oxygen supply with back-up
risk of occupational injury and death for providers related to the inherent risks associ- Transport pack with emergency drugs and supplies
ated with the mode of transportation, design limitations of the vehicles and vulnerability
associated with delivering care in the transport environment. PATIENT
Stabilized on transport stretcher
Prehospital Transport Monitors in place and operational/Equipment secured
Prehospital care is provided by emergency medical personnel in the setting of out of
hospital illness or injury. The scope of care, standardized practices and equipment are Ventilation adequate/Assessment of gas exchange if using trans-
specialized for the clinical environment and may differ from those employed during port ventilator
secondary transport. Prehospital transport typically occurs in the setting of an integrated Appropriate sedation/neuromuscular blockade (if indicated)
emergency medical system. Triage decisions regarding the transport destination of a
particular patient are important. Available evidence demonstrates improved outcomes Measures to prevent heat loss
for patients triaged to dedicated centers for conditions including trauma, acute coro- COMMUNICATION
nary syndromes and stroke. Under-triage, the referral of patients who may benet from
specialized care erroneously to lower acuity centers, may adversely affect outcome. Transfer documents prepared
Likewise, over-triage, transferring patients not needing specialized care to dedicated Full physician and nursing report to receiving location
centers, may result in overcrowding and misuse of resources. The role of pre-hospital
transport using helicopter emergency medical systems (HEMS) over ground transport DOCUMENTATION
for patients with major trauma has been a widely debated subject with recent data sug- Vital signs/Notations of events during transport
gesting an advantage for HEMS. Controversies remain in several areas of prehospital
transport including the benet of stabilization of patients at the scene via advanced life Adverse Events/Process Improvement
support (stay and play) versus rapid transport to an appropriate facility (scoop and
run). Other controversies include the role of advanced airway management, the compo- tions in the United States stipulate that hospitals receiving funding from Medicare have
sition and training of team members and the precise elements of HEMS that confers a duty to evaluate and provide treatment to stabilize patients with an emergency medi-
benet. These elements include speed of transport, team composition, team expertise, cal condition regardless of citizenship, legal status or ability to pay as initially describe
and appropriate, specic therapeutic interventions. in the Consolidated Omnibus Budget Reconciliation Act (COBRA) and later rened in
the Emergency Medical Treatment and Active Labor Act (EMTALA). Considerations
for choosing a mode of transport include the urgency of transport, time to mobilize the
Inter-hospital Transport transport team and vehicles, geographical factors, weather, trafc conditions and cost.
Interfacility transport is most commonly considered to allow critically ill patients to In general, ground transport is suitable for many patients and has the advantage of lower
access a higher level of care or to receive treatment for conditions requiring specic cost and is less likely to be affected by inclement weather. Rotary wing transport can be
specialty expertise or procedures not available at the referring facility. Federal regula- considered for transport distances of 50 to 200 miles and in situations where terrain fac-
dedicated transport teams may incur increased direct costs to healthcare organizations.
Table 4.2 Adverse Events Associated with Transport An increasing number of procedures frequently required by ICU patients including
Cardiovascular Events Hypotension tracheostomy and percutaneous endoscopic gastrostomy can be performed safely at the
Hypertension bedside avoiding the need for patient transport and the associated allocation of resourc-
Dysrhythmia es.
Loss of Vascular Access
Cardiac Arrest
Death Table 4.3 Considerations for Interhospital Transport
Administrative - informed consent obtained from patient or legally
Respiratory Events Hypoxia authorized representative
Hypercarbia - if consent cannot be obtained, the reason should be
Bronchospasm documented along with the indication for transport
Pneumothorax - a written order for transfer is recommended
Respiratory Arrest
Inadvertent Extubation Coordination & Commu- - referring physician communicates with accepting
Increased Risk of VAP nication physician to conrm acceptance of the patient, avail-
ability of required resources and to give detailed report
of patient condition
Neurological Events Agitation - designate a physician to assume responsibility for
Altered Mental Status treatment during transport if no physician is on the
Intracranial Hypertension transport
- determine the mode of transport
Equipment & Medical Supply Events Equipment Failure - nursing report is performed by a nurse at the re-
Improper Use of Equipment ferring facility or a member of the transport team
Battery Failure - send/deliver a copy of the medical record along with
Inadequate Medical Supplies pertinent studies to the receiving facility
Oxygen Failure Team Composition - team composition is variable and often based on
Critical Medications/ Supplies/ Equipment patient acuity
Monitoring & Equipment - Minimum monitoring includes continuous pulse
oximetry, electrocardiogram, and regular measurement
Staff & Administration Related Events Inadequate Staff of blood pressure and respiratory rate.
Communication and Liaison Problems - advanced monitoring including capnography, invasive
hemodynamic monitoring and intracranial pressure
Miscellaneous Events Hypothermia monitoring can be considered as needed.
- Basic equipment includes airway adjuncts, physiologic
tors limit ground access. Fixed wing transport may be considered for distances greater monitors, suction, infusion devices and agents for
resuscitation and maintenance of vital functions.
than 200 miles. Important aspects of inter-hospital transport are summarized in Table 3. - transport ventilators should be utilized for intubated
The optimal team composition, team training, skills verication, practice specic algo- patients
rithms, implementation of crew resource management principles and effect of process - all equipment and supplies are checked before
improvement initiatives on patient outcome are not well dened. transport including available IV uids, drips and blood
Intrahospital Transport Patient Factors and Prep- - Resuscitation and Stabilization via CAB approach
Movement of patients from the intensive care unit to other locations within the hospi- aration - hemorrhage controlled
tal is most often performed to obtain diagnostic radiographic studies or for operative (Packaging the Patient) - blood pressure stabilized
- C-spine immobilized (trauma)
procedures. The relative risk of transport should be weighed against the potential benet - fractures splinted
derived from the anticipated diagnostic or therapeutic intervention. The goal as with any - Is there a need to control the airway?
other transport is to maintain the same level of monitoring and supportive care that the - consider transport time and potential alterations in
patient receives in the ICU. As discussed previously, a variety of adverse events have airway integrity and gas exchange with transport
been reported during intrahospital transport and this represents an area for potential - is there a need for increased IV access or invasive
improvement in patient safety. There is evidence that dedicated transport teams may monitoring?
reduce the incidence of adverse events during transport while having benecial effects - is there a need for nasogastric decompression,
on ICU stafng, job satisfaction and time spent in transport related activities. However, urinary catheter placement or tube thoracostomy?

Available data suggest that critically ill and injured patients can be transported safely Questions
in a variety of transport environments with proper understanding and mitigation of
4.1 Interhospital transport is MOST LIKELY to be performed in which of the following scenarios?
risk. However, the transport environment remains associated with an increased risk for
adverse events. A number of factors likely inuence the safety, efcacy and efciency A. Transfer of an unstable patient with urosepsis who is unable to pay for treatment in the
of the transport process, but these are not yet fully dened. emergency department at the referring facility
B. Transfer of an inpatient with acute kidney injury and hyperkalemia from a hospital with-
out a hemodialysis service to a hospital with availability of renal replacement therapy
C. Transfer of a patient with an acute coronary syndrome from a regional cardiac center to
a nearby community hospital
References D. Transfer of a trauma patient who has tachycardia and orthostatic hypotension upon ar-
1. Beckmann U, Gillies DM, Berenholtz SM, Wu AW, Pronovost P: Incidents relating to rival to the emergency department of a community hospital
the intra-hospital transfer of critically ill patients. An analysis of the reports submitted to
the Australian Incident Monitoring Study in Intensive Care. Intensive Care Med 2004; 30:
1579-85 4.2 Which of the following is the MOST LIKELY reason transport ventilators are recommended
2. Blakeman TC, Branson RD: Inter- and Intra-hospital Transport of the Critically Ill. for use in patient transport?
Respir Care 2013; 58: 1008-23
3. Brice JH, Studnek JR, Bigham BL, Martin-Gill C, Custalow CB, Hawkins E, Morrison A. Transport ventilators are capable of maintaining the same ventilator parameters as criti-
LJ: EMS Provider and Patient Safety during Response and Transport: Proceedings of an cal care ventilators
Ambulance Safety Conference. Prehosp Emerg Care 2012; 16: 3-19 B. Transport ventilators use special batteries that do not require frequent recharging
4. Droogh JM, Smit M, Hut J, de Vos R, Ligtenberg JJ, Zijlstra JG: Inter-hospital trans- C. All transport ventilators use less oxygen than simple hand bag ventilation
port of critically ill patients; expect surprises. Crit Care 2012; 16: R26 D. Transport ventilators may prevent harmful hypoventilation or hyperventilation of pa-
5. Fanara B, Manzon C, Barbot O, Desmettre T, Capellier G: Recommendations for the tients with increased intracranial pressure
intra-hospital transport of critically ill patients. Crit Care 2010; 14: R87
6. Galvagno SM,Jr, Haut ER, Zafar SN, Millin MG, Efron DT, Koenig GJ,Jr, Baker SP,
Bowman SM, Pronovost PJ, Haider AH: Association between helicopter vs ground emer- 4.3 Which of the following statements regarding intrahospital transport is MOST LIKELY true?
gency medical services and survival for adults with major trauma. JAMA 2012; 307:
1602-10 A. It is impossible to maintain the same monitoring and supportive care received in the
7. Ligtenberg JJ, Arnold LG, Stienstra Y, van der Werf TS, Meertens JH, Tulleken JE, ICU due limited capabilities of transport equipment
Zijlstra JG: Quality of interhospital transport of critically ill patients: a prospective audit. B. Additional medical supplies do not need to be carried if the transport location is on the
Crit Care 2005; 9: R446-51 same hospital oor as the ICU
8. Pauldine R, Gerold K: Transport of the Critically Ill Patient. Contemporary Critical C. Patient movement is associated with an increased risk of ventilator associated pneumo-
Care 2008; 5: 1-12 nia
9. Schwebel C, Clech C, Magne S, Minet C, Garrouste-Orgeas M, Bonadona A, Dumenil D. Adverse events are rare during intrahospital patient transport
AS, Jamali S, Kallel H, Goldgran-Toledano D, Marcotte G, Azoulay E, Darmon M, Ruckly
S, Souweine B, Timsit JF, the OUTCOMEREA Study Group: Safety of Intrahospital Trans-
port in Ventilated Critically Ill Patients: A Multicenter Cohort Study*. Crit Care Med 2013;
41: 1919-28
10. Warren J, Fromm RE,Jr, Orr RA, Rotello LC, Horst HM, American College of Criti-
cal Care Medicine: Guidelines for the inter- and intrahospital transport of critically ill
patients. Crit Care Med 2004; 32: 256-62

5. Cardiopulmonary Resuscitation
Ebony J Hilton MD

Key Points 68yo WM with PMHx of HTN, Hyperlipidemia, IDDM noted to collapse and
become unresponsive while playing golf. Patients friends state that he
Anesthesiologists need to recognize the signs
was complaining of chest tightness prior to the event, and after nding no
pulse, they initiated CPR. Emergency personnel arrived within 3 minutes
and symptoms of a dysrhythmia as well as and performed debrillation with 200J when rhythm analysis revealed
understand the pathophysiology, therapeutic ventricular brillation. A palpable pulse is noted after debrillation,
management, and direction of care following although the patient remains unresponsive. He is then intubated and
return of spontaneous circulation. transported to the nearest hospital for further management.

Adequate chest compressions is now

considered the priority of any resuscitative
initiative, followed by establishment of airway
and providing breaths

Post-cardiac arrest care requires as much

vigilance as the resuscitative measures during
the arrest.
The skills acquired while training to become a critical care physician affords one to be of great resource dur-
ing times of uncertainty; this holds true regardless of location both in and out of the hospital. The time when
this is most evident is when someone experiences a cardiac arrest or other life threatening arrhythmia. It is
therefore of great importance for us to not only recognize the signs and symptoms of dysrhythmia but also
understand the pathophysiology, therapeutic management aimed at correcting the disease state, and direction
of care following return of circulation.

The most daunting of tasks can be determination of the primary insult but in an unstable situation this should
not delay initiation of cardiopulmonary resuscitation. Calling a code, establishing a secured airway, perform-
ing chest compressions (30:2) with minimal interruptions, placing external debrillator pads for EKG analysis
and possible electric conversion should occur almost simultaneously. This typically requires multiple person-
nel to be involved. In addition to the aforementioned steps, one must establish intravenous access and obtain
labs to help determine potential causes of the dysrhythmia. It is therefore paramount for a code leader to be
identied and serve as a director to coordinate these events to happen as seamlessly as possible.

Return of circulation and stabilization of the patient is only half of the battle. Post-cardiac arrest care requires
as much vigilance as the resuscitative measures prior. Optimize ventilation and oxygenation (SpO2>94%,
PEtCO2 35-40mmHg). Treat hypotension with uids and vasoactive agents, and work-up potential contribut-
ing factors with review of EKG, CXR, and labs (ABG, BMP, CBC, glucose, coagulation panel, etc.). Con-
sider induced hypothermia if patient remains unresponsive despite return of circulation, II. Airway
and coronary reperfusion interventions if there is a high likelihood of STEMI or MI. A. Management
Unfortunately, despite these measures, morbidity and mortality remain high following 1. Examine oral pharynx for foreign body.
cardiac arrest with most related to neurologic and cardiac injury. It has been shown,
however, that 20-50% of comatose patients who presented to the hospital following 2. Administer 100% FiO2 whenever possible.
cardiac arrest may have good one-year neurological outcome. Therefore admitting 3. Monitor EtCO2 if possible.
the resuscitated patient to an ICU with advanced neurologic monitoring may help to 4. Supraglottic Airway Techniques: Increased risk of gastric distension & aspiration
improve long term prognosis. a. Mouth to Mouth
b. Bag Mask
c. Oral/Nasal airway
Resuscitative Algorithm d. Laryngeal Mask Airway device
Studies have revealed that providing circulation to a patient in cardiac arrest is the 5. Denitive Airway: Allows for continuous ventilation during CPR
primary determinant of improved outcome. Therefore initiation of adequate chest a. Endotracheal Intubation
compressions is now considered the priority of any resuscitative initiative, followed by
establishment of airway and providing breaths. To stress the importance of this order the b. Tracheostomy
American Heart Association promotes the use of the acronym CAB.
III. Breathing
I. Circulation A. Position patient for optimal ventilation: jaw thrust, head tilt, chin lift.
A. Initial assessment should include determination of pulsatile ow, underlying B. Rate:
rhythm, and heart rate. 1. Supraglottic Airway: [30:2] compressions to breath ratio
1. Pulse: Check carotid/radial/femoral sites for pulse. If questionable do not delay 2. Denitive Airway: uninterrupted 10-12 breaths per minute
resuscitative measures, i.e. CPR.
2. Rhythm: Place debrillator pads for analysis. IV. Debrillation
a. Shockable Rhythms: Ventricular brillation, Ventricular Tachycardia, Atrial A. Safety:
brillation, Atrial Flutter, Re-entry SVT 1. Make sure no one is touching the patient or connecting surfaces during delivery
i. Perform direct current cardioversion as soon as possible (120-200J with of shock.
biphasic device. B. Timing:
b. Unshockable Rhythms: Pulseless Electrical Activity, Asystole 1. It should occur as soon as possible for any shockable rhythm, optimally within 3
3. Rate: If pulse is present but patient is bradycardic (HR< 60bpm), consider minutes of diagnosis.
transcutaneous pacing. a. Shockable Rhythms: Ventricular brillation, Ventricular Tachycardia, Atrial
B. Chest Compressions should be performed until a debrillator is available and brillation, Atrial Flutter, Re-entry SVT
ready to deliver a shock or indenitely if the rhythm is determined unshockable. i. Perform direct current cardioversion as soon as possible (120-200J with
1. Technique: Place patient on a hard surface. Use the heel of your hand in the biphasic device).
center of the chest, along nipple line, to provide compressions at a depth of ~2in at b. Unshockable Rhythms: Pulseless Electrical Activity, Asystole
a rate of 100 compressions per minute.
2. Compression to Breath ratio: [30:2]. Watch for chest rise and fall with each
rescue breath lasting 1 second. If there is no chest rise then consider patient V. Following Return of Circulation (ROSC)
positioning being an issue and provide jaw thrust, head tilt, chin lift, oral/nasal A. Management
airway, LMA, or intubate if experts of airway management are available. 1. Optimize Ventilation & Oxygenation (SpO2>94%, PEtCO2 35-40mmHg)
a. All of these maneuvers should occur with priority being place on limiting 2. Treat Hypotension: Fluids/Vasopressors
duration of interruptions to compressions. B. Work-up for triggering event
b. If patient is intubated then continuous ventilation can occur at a rate of 10-12 1. History and Physical
breaths per minute via an Ambu-bag and 100% FiO2. Monitor for EtCO2. a. Review Past Medical History
3. Pulse Check: Assess for pulse at the completion of a full CPR cycle [30:2 x 5 i. Risk factors for cardiac insult: HTN, HL, DM, male, CHF, CRF, previous
cycles] and after cardioversion. stroke
a. If feasible a pulse should be continuously monitored (A-line wave form or ii. Risk factors for pulmonary embolus: cancer, smoking, obesity, recent
rescuer palpating femoral/radial sites), or monitoring of EtCO2 in order to ensure surgery, pregnancy
adequate chest compressions.
iii. Risk factors for neurologic insult which can often present with dysrhymias:

HTN, chronic headaches, trauma, intrancranial hemorrhage e. Recent multicenter study showing that there may be no signicant
b. Recent Medications difference between 36C versus 33C in terms of favorable outcomes, but that
i. Every medicine has a side-effect and their interactions can result in the active prevention of hyperthermia may be the key
dysrhythmia. 2. Coronary Reperfusion
c. Recent Events a. Consider if high likelihood of STEMI or MI.
i. Surgery: Consider volume status/hemorrhagic shock, pulmonary embolus,
tamponade (CABG or intrathoracic cases), pneumothorax, sepsis. Diagnostic and Treatment Algorithms
ii. Trauma: Consider volume status/hemorrhagic shock, pulmonary embolus, The following algorithms serve as reference in the diagnosis and pharmacologic man-
tamponade (CABG or intrathoracic cases), pneumothorax (is chest tube agement of the most common arrhythmias encountered in the ICU. They are designed
kinked?). to be reviewed independently of each other.
iii. Intubation: Consider misplaced endotracheal tube (conrm bilateral breath
sounds, EtCO2 monitoring), induction agents (succinyl choline can reult in A. Bradyarrhythmia:
hyperkalemia). 1. Types:
2. Review Labs a. Sinus Bradycardia: decreased number of impulses arising from SA to AV node
i. ABG, CMP(comprehensive metabolic panel), CBC, Coag, Glucose, Cardiac b. 1st degree AV block: Slowed conduction through the AV node
c. 2nd degree AV block: Missed beats due to intermittent AV block
b) Often times hypoxia, acidosis, hypo/hyperkalemia, and hypoglycemia are
initiating culprits. i. Type I (Wenckebach/Mobitz I)
3. Imaging/Studies ii. Type II (Mobitz II)
a. CXR d. 3rd degree AV block: complete AV nodal block
i. Look for signs of pneumothorax or tamponade. 2. Denition:
b. Echo a. Stable Bradyarrhythmia: HR <60bpm and asymptomatic
i. Focal wall motion abnormalities suggestive of ischemic insult b. Unstable Bradyarrhythmia: HR <60bpm and signs/symptoms of end organ
ii. Global hypokinesis suggestive of stunned myocardium
i. Hypotensive, complains of chest discomfort, shortness of breath,
iii. Dilated right ventricle suggestive of pulmonary embolus lightheadedness, nausea/vomiting, altered level of consciousness/mentation,
iv. Pericardial effusion and tamponade diaphoretic, CXR with signs of acute heart failure (pulmonary edema) or
c. EKG other signs of shock
i. Compare to prior study 3. Common Etiologies:
ii. ST elevations: a. Medications
a) Diffuse: pericarditis i. negative chronotropes (digoxin, beta blockers, calcium channel blockers),
b) Anterior MI: leads V1-V4 Alpha1 Agonists (phenylephrine), antiarrhythmic drugs (amiodarone),
c) Inferior MI: II, III, AVF (Q waves and ST elevations) antipsychotic meds (lithium)
d) Lateral MI: I, AVL, V5, V6 b. Electrolyte disturbances: hyperkalemia, hypermagnesaemia,
e) Right Heart Strain: inverted T waves V1-V3, right atrial enlargement c. Disease processes: elevated ICP, acute MI, increased vagal activity,
hypothyroid, protracted hypoxia
f) Pulmonary Embolus: S1Q3T3
4. Management:
C. Procedures/Intervention:
a. History and Physical exam: CABs
1. Induced Hypothermia
i. Auscultate for heart sounds and palpation for distal pulses.
a. Recommended if patient remains unresponsive despite return of
circulation after out-of-hospital VF cardiac arrest. ii. Evaluate patency of airway.
b. Consider if patient remains unresponsive after return of spontaneous iii. Supply supplemental oxygen and provide respiratory support as required to
circulation after in-hospital cardiac arrest of any initial rhythm or after out- maintain SpO2>94% and PEtCO2 of 35-45mmHg.
of-hospital cardiac arrest with an intial rhythm of pulseless electric activity or iv. History: presenting illness, PMHx, medications, allergies, recent labs
asystole. (CBC, BMP, ABG, etc.)
c. Cool patient to 32-34C for12-24 hours b. Monitors:
d. Avoid active rewarming in comatose patients who spontaneously are mildly i. Continuous EKG, pulse oximetry, blood pressure monitoring, 12 lead EKG
hypothermic (>32C) c. Treatment: Correct reversible causes

i. Stable Bradyarrhythmia: a. Stable Tachyarrhythmia: HR >100bpm and asymptomatic
a) Continue to monitor and observe for hemodynamic stability. b. Unstable Tachyarrhythmia: HR >100bpm & signs/symptoms of end organ
ii. Unstable Bradyarrhythmia: Consider cardiology consult insult
c) Interventions: i. Hypotensive, ST segment changes on EKG, complains of chest discomfort,
1) Place patient in trendelenburg position. Shortness of breath, lightheadedness, nausea/vomiting, altered level of
consciousness/mentation, diaphoretic, CXR with signs of acute heart failure
2) Establish IV access (bolus 500cc to 1L crystalloid). (pulmonary edema) or other signs of shock
d) Medication: 3. Common Etiologies:
3) 1st line: Atropine IV a. Medications
i) Initial: 0.5mg bolus IV i. Stimulants (Nicotine, caffeine, cocaine), anticholinergics, antihistamines,
ii) Redose: may repeat 0.5mg IV every 3-5mins up to maximum of 3mg theophylline, digitalis toxicity, sympathomimetics (epinephrine, ephedrine,
4) 2nd line: Chronotropic Augmentation dopamine)
i) Dopamine IV infusion 2-10mcg/kg/min b. Electrolyte disturbances: hypokalemia, hypomagnesemia, hypocalcemia
ii) Epinephrine IV infusion 2-10mcg/kg/min c. Stressors: pain, fever, anxiety, hypovolemia, hypoxia, hypercarbia
e) Transcutaneous/Transvenous pacing d. Disease processes: hyperthyroid, sepsis, pulmonary embolus, myocardial
infarction, COPD, pheochromocytoma, heart failure
B. Tachyarrhythmia: 4. Management:
1. Types: a. History and Physical exam: CABs
a. Regular Narrow Complex Tachycardias: i. Auscultation for heart sounds and palpation for distal pulses
i. Sinus Tachycardia: increased no. of impulses arising from SA to AV node ii. Evaluate patency of airway
ii. Re-entry Supraventricular Tachycardia (SVT): accessory pathway between iii. Supply supplemental oxygen and provide respiratory support as required to
atria and ventricle that can allow for a combination of anterograde and maintain SpO2>94% and PEtCO2 of 35-45mmHg
retrograde conduction of impulses through to the AV node iv. History: presenting illness, PMHx, medications, allergies, recent labs
b. Irregular Tachycardias (CBC, BMP, ABG, etc.)
i. Atrial Fibrillation: AV node receives signals from multiple foci (commonly b. Monitors:
originating near the root of pulmonary veins in L. Atrium), each ring i. Continuous EKG, pulse oximetry, blood pressure monitoring, 12 lead EKG
disorganized c. Treatment: Correct reversible causes
electrical impulses (usually 400-600bpm) that the AV node tries to lter out i. Unstable Tachyarrhythmia with Positive Pulses
but ultimately still allows conduction of more beats at varying rates and in an
irregular pattern to the Ventricles a) Interventions:
ii. Atrial Flutter: Reentry pathway (usually in R. Atrium) that leads to a 1) Establish IV access: consider sedation (versed, fentanyl)
localized self-perpetuating loop of AV node activation in a regular pattern 2) Consider Expert Consultation
(~300bpm). Due to the xed, regular input of signals received, and the b) Synchronized Cardioversion: Everyone stand clear
longer refractory period of the AV node, not all impulses will be conducted. 1) Narrow, Regular QRS (<0.12s):
Results in presence of AV block (2:1, 3:1, 4:1, etc.) and predictable heart rates i) Initial: 50-100J
(150bpm, 100bpm, 75bpm, etc.)
ii) Failed: shock increase in a stepwise fashion
iii. Multifocal Atrial Tachycardia (MAT): Thought to result from either one o (50, 100, 150, 200J)
foci impulse traveling from atria to AV node via multiple routes OR multiple
foci conducting impulses through one route. EKG must show P waves of at 2) Narrow, Irregular QRS (<0.12s):
least three different morphologies for diagnosis to be made. i) Initial: 120-200J Biphasic; 200J Monophasic
c. Wide-complex tachycardia: ii) Failed: shock increase in a stepwise fashion
i. Monomorphic VT: Within a Ventricle (Usually at origin of R. Ventricular o (120, 150, 200J)
Outow Tract) there is either a single foci that has increased automaticity or a 3) Wide, Regular QRS (>0.12s):
single reentry circuit leading to repetitive depolarizations i) 100J Biphasic
ii. Polymorphic VT: Multiple foci within the ventricle res impulses or ii) Failed: shock increase in a stepwise fashion
multiple reentry pathways lead to repetitive depolarizations and EKG shows o (100, 150, 200J)
QRS complexes of varying morphology. d. Unsynchronized Cardioversion: Everyone stand clear
2. Denition: i. Wide, Irregular QRS (>0.12s):
a) 150J Biphasic a) Esmolol:
b) Failed: shock increase in a stepwise fashion 1) Initial: 0.5mg/kg IV bolus
o (150, 200J) 2) Redose: 0.5mg/kg IV bolus if no response within 2 min of initial bolus
e. Medication: 3) Infusion: 50-300mcg/kg/min
i. Adenosine IV: Only if Narrow QRS Complex b) Metoprolol:
a) Initial: 6mg rapid IV bolus 1) Initial: 5mg IV over 1-2min
b) Redose: 12mg IV bolus if no response from initial bolus within 1-2 min 2) Redose: 5mg IV q5min to max dose of 15mg
iii. Calcium Channel Blocker:
5. Stable Tachyarrhythmia w/ Regular, Narrow QRS (<0.12s): a) Diltiazem:
[Likely Sinus Tachycardia or Reentry SVT] 1) Initial: 0.25mg/kg IV bolus over 2min
a. Interventions: 2) Redose: 0.35mg/kg in 15min
i. Establish IV access 3) Infusion: 5-15mg/h
ii. Vagal Maneuvers ii. Antiarrhythmic:
a) Carotid Massage (listen to rule out carotid bruit rst, perform on one side a) Amiodarone IV:
at a time)
1) Initial: 150mg IV over 10min
b) Ask patient to perform Valsalva maneuver
2) Redose: 150mg IV over 10min q10min if rhythm recurs
iii. Consider Expert Consultation
3) Infusion: 1mg/min for 1st 6h, followed by 0.5mg/min
b. Medication:
i. Adenosine IV
7. Stable Tachyarrhythmia w/ Regular, Monomorphic Wide QRS (>0.12s):
a) Initial: 6mg rapid IV bolus
a. Interventions:
b) Redose: 12mg IV bolus if no response from initial bolus within 1-2 min
i. Establish IV access
iii. Beta-Blocker:
ii. Consider Expert Consultation
a) Esmolol:
b. Medication:
1) Initial: 0.5mg/kg IV bolus
i. Adenosine IV:
2) Redose: 0.5mg/kg IV bolus if no response within 2 min of initial bolus
a) Initial: 6mg rapid IV bolus
3) Infusion: 50-300mcg/kg/min
b) Redose: 12mg IV bolus if no response from initial bolus within 1-2 min
b) Metoprolol:
iii. Antiarrhythmic:
1) Initial: 5mg IV over 1-2min
a) Amiodarone IV:
2) Redose: 5mg IV q5min to max dose of 15mg
1) Initial: 150mg IV over 10min
iii. Calcium Channel Blocker:
2) Redose: 150mg IV over 10min q10min if rhythm recurs
a) Diltiazem:
3) Infusion: 1mg/min for 1st 6h, followed by 0.5mg/min
1) Initial: 0.25mg/kg IV bolus over 2min
b) Procainamide IV: Avoid if prolonged QT/CHF
2) Redose: 0.35mg/kg in 15min
1) Initial: 20-50mg/min until rhythm abates or hypotension occurs, QRS
3) Infusion: 5-15mg/hr duration increases >50% or max dose of 17mg/kg given
2) Infusion: 1-4mg/min
6. Stable Tachyarrhythmia w/ Irregular, Narrow QRS (<0.12s): c) Sotalol IV: Avoid if prolonged QT
Likely Atrial brillation, Atrial utter, or Multifocal Atrial Tachycardia
3) Initial: 1.5mg/kg IV over 5min
a. Interventions:
i. Establish IV access
C. Pulseless Rhythms:
ii. Vagal Maneuvers
1. Types:
a) Carotid Massage (rule out carotid bruit 1st, perform on one side at a time)
a. Shockable Rhythms:
b) Ask patient to perform Valsalva maneuver
i. Ventricular Fibrillation: Multiple sites of microreentry pathways within the
iii. Consider Expert Consultation ventricle that results in electrical pattern with no obvious P wave and lack of
b. Medication: properly formed QRS complex.
i. Beta-Blocker: Avoid in COPD/CHF
ii. Pulseless Ventricular Tachycardia: Within a ventricle there is either a patient.
single foci that has increased automaticity or a single reentry circuit leading 2) Begin CPR Until Debrillator Available
to repetitive depolarizations causing an inability to generate adequate i) Conrm placement of CPR board under patient.
coordination for cardiac output.
ii) 30 compressions:2 breaths
b. Non-Shockable Rhythms:
iii) Rate of 100 compression/min
i. Asystole: Complete absence of electrical activity on EKG
iv) Can attempt to establish denitive airway but this should not delay
ii. Pulseless Electrical Activity (PEA): Evidence of electrical activity on EKG CPR.
but no resulting mechanical cardiac output, i.e. no pulse or measurable blood
pressure 3) Debrillation
2. Denition: i) Continue CPR until debrillator pads attached and ready for rhythm
a. Shockable Rhythm: Underlying arrhythmia stems from chaotic ring of
electrical impulses. Goal of Cardioversion is to supply a shock to reset ii) Tell staff to stand clear of patient and contacting surfaces.
(depolarize) the electrical conduction system so that when the heart again iii) Deliver initial shock of 120-200J.
repolarizes the normal electrical conduction system (SA, AV nodes, etc.) can 4) Resume CPR
resume command. i) Complete 5 cycles (~2min)
b. Non-Shockable Rhythm: Underlying arrhythmia is not secondary to 5) Rhythm Analysis: EKG ndings and Pulse Analysis
disorganized electrical impulses but rather the lack of electrical input or i) Return of Circulation:
electromechanical dissociation. Therefore, applying an electrical shock to reset
(depolarize the system) would not be of benet. Denition:
Palpable pulse or arterial pressure tracing evident with intra-
arterial monitor
3. Common Etiologies:
Sustained increase in PEtCO2
a. Medications: Toxins (overdose on beta blockers, calcium channel blockers,
opioids, etc.) Treatment:
b. Electrolyte disturbances: hyper/hypokalemia, Acidosis Optimize Ventilation & Oxygenation (SpO2>94%, PEtCO2 35-
c. Stressors: hypovolemia, hypoxia, hypothermia
Treat Hypotension: Fluids/Vasopressors
d. Disease processes: tension pneumothorax, cardiac tamponade, pulmonary
embolus, myocardial infarction Work-up
4. Management: Labs: ABG, BMP, CBC, glucose
a. History and Physical exam: CABs Procedures/Intervention:
i. Auscultation for heart sounds and palpation for distal pulses Induced Hypothermia: Consider this if patient remains
unresponsive despite return of circulation.
ii. Evaluate patency of airway
Coronary Reperfusion Tx: Consider if high likelihood of STEMI
iii. Supply supplemental oxygen and provide respiratory support as required to or MI.
maintain SpO2>94% and PEtCO2 of 35-45mmHg
Consult Cardiology
iv. History: presenting illness, PMHx, medications, allergies, recent labs
(CBC, BMP, ABG etc)
b. Monitors: ii. Shockable Rhythm: V-Fib or Pulseless V-Tach
i. Continuous EKG, pulse oximetry, blood pressure monitoring, 12 lead EKG a) Debrillate 100-200J
c. Treatment: Correct reversible causes b) Resume CPR x5 cycles (~2min)
i. Shockable Pulseless Arrhythmias: 1) During CPR give Epinephrine 1mg IV q3-5 min.
Likely Ventricular Fibrillation or Ventricular Tachycardia c) Repeat Rhythm analysis
a) Interventions: 1) If Shockable Rhythm, repeat these steps above.
1) Call Code 2) If Return of Circulation, follow previously outline recs.
i) Ask for Code Cart with Debrillator. 3) For Non-Shockable Rhythm, see below.
ii) Have available staff obtain IV access and attach debrillator pads on

iv. Non-shockable Rhythm: Asystole or PEA c) Repeat Rhythm analysis
a) CPR x 2min 1) If Shockable rhythm, repeat outlined these steps above.
1) Give Epinephrine 1mg 3-5min during CPR. 2) If Return of Circulation, follow previously outline recs.
b) Repeat Rhythm Analysis 3) For Non-Shockable Rhythm, see below.
1) If Non-Shockable Rhythm, repeat these steps above 4) Non-Shockable Rhythm: Asystole or PEA
2) If Return of Circulation, follow previously outline recs d) Resume CPR and repeat above steps
3) If Shockable Rhythm, follow previously outline recs

iii. Non-Shockable Pulseless Arrhythmias:

Likely Asystole or Pulseless Electrical Activity (PEA)
a) Interventions: Reference:
1) Call Code 1. ACLS: Cardiac Arrest, Arrhythmias, and Their Treatment, pocket reference card.
American Heart Association, 2011.
i) Ask for Code Cart with Debrillator. 2. Chung M: Cardiac surgery: postoperative arrhythmias. Critical Care Medicine 2000;
ii) Have available staff obtain IV access and attach debrillator pads on 28: 136-44.
patient. 3. McEvoy M, Schaefer J, Choi Y, Crumpler M, Matos J: 4-Step Approach to ACLS Man-
agement, pocket reference card. Medical University of South Carolina, 2011.
2) Perform CPR for 2 min 4. Melduni R, Koshino Y, Shen W: Management of arrhythmias in the perioperative set-
i) Conrm placement of CPR board under patient. ting. Clinics in Geriatric Medicine, 2012; 28:729-43.
5. Nielson N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C et al: Targeted
ii) 30 compressions:2 breaths temperature management at 33 C versus 36 C after cardiac arrest. N Engl J Med, 2013:
iii) Rate of 100 compression/min 369, 2197-2206.
iv) Can attempt to establish denitive airway, but this should not delay
v) Give Epinephrine 1mg IV q3-5min while performing CPR.
3) Rhythm Analysis: EKG ndings and Pulse Analysis
i) Return of Circulation:
Palpable pulse or arterial pressure tracing evident
Sustained increase in PEtCO2
b) Treatment:
5.01 Immediately following elective intubation of a 24yo paraplegic male for airway protec-
1) Optimize Ventilation & Oxygenation (SpO2>94%, PEtCO2 35- tion during endoscopy, he is noted to be in asystole. Induction agents included lidocaine,
40mmHg) propofol, succinylcholine, and fentanyl. What is the correct sequence of events that should
occur during this code?
2) Treat Hypotension: Fluids/Vasopressors E. Conrm placement of ETT, begin chest compressions, give Epi/Calcium/Bicarbonate/
c) Work-up Insulin&Glucose
F. Begin Chest compressions, give Epi, cardiovert as soon as debrillator is available,
1) EKG, CXR conrm placement of ETT
2) Labs: ABG, BMP, CBC, glucose G. Begin Chest compressions, Conrm placement of ETT, give epi/calcium/bicarbonate/
d) Procedures/Intervention: H. Begin Chest compressions, give Epi, Conrm placement of ETT
1) Induced Hypothermia: Consider this if patient remains unresponsive 5.02 What is the most common cause of cardiac arrest in the pediatric population?
despite return of circulation A. Congenital cardiac malformation
i) Coronary Reperfusion Tx: Consider this if high likelihood of STEMI B. Asphyxia
or MI C. Hypovolemia
D. Ischemic insult
e) Consult Cardiology
5.03 What is the most reliable method of detecting proper Endotracheal Tube placement?
A. Bilateral breath sounds
vi. Shockable Rhythm: V-Fib or Pulseless V-Tach B. ETCO2
a) Debrillate 100-200J C. Ascultation over stomach
D. Misting within endotracheal tube
b) Resume CPR x5 cycles (~2min)
1) During CPR give Epinephrine 1mg IV q3-5 min.
6. Ethical Issues in the ICU
Jessica Reardon DO and Theresa Hartsell MD PhD

Key Points A 55-year-old male collapsed at home and was sent to the emergency
department. Upon arriving to the hospital, he was found unresponsive with
The four principles of medical ethics are a Glascow Coma Score of 6. He was intubated, stabilized, and underwent a
CT scan which showed a massive intracerebral hemorrhage. After emergent
autonomy, beneficence, non-maleficence, and
craniectomy for cerebral decompression, he was sent to the ICU. It has
justice. been ve days since the event with little change in his clinical picture.
A family meeting will occur with physicians, nurses, and social work to
A patient should be assessed for capacity discuss goals of care with his wife and daughters.
to make decisions. If they are not capable a
surrogate decision maker should be appointed. During the family meeting, the care team discovers that the patient did
not have an advance directive. However, his wife, who is now acting as
Withdrawal of support is not withdrawal of his surrogate decision maker, states that her husband would never have
care and patients have the right to refuse or wanted to live chronically on the ventilator with articial nutrition if there
accept life- sustaining treatments. was little chance for recovery. After being updated regarding his overall
clinical picture, the wife makes the difcult decision to withdraw ventilator
The Principle of Double Effect states that
an intervention is allowed if the intended Prior to withdrawal of ventilator support, the patient is examined for
outcome is in itself good even if it may have neurologic function. It is determined that the patient can be clinically
undesirable side effects. diagnosed as having brain death. After informing the family, his wife
says that her husband is an organ donor and would want to donate his
organs to others.

Ethical issues occur frequently in the intensive care unit. For patients who are critically ill or near the end of
life, difcult decisions regarding their treatment plan often need to be made. When approaching discussions
with the family of a critically ill patient, a care plan should generally be described within 48 hours after ad-
mission. There are four core principles in medical ethics that provide a framework to guide the care process
of a medical provider: autonomy, benecence, non-malecence, and justice. (Table 6.1)

After the initial conversation, a discussion should occur about the patients beliefs, values, and goals. Updates
should be provided to both the patient and his or her family. This will help to build a relationship between the
care team (physicians, nurses, social workers, etc.) and the family along with identifying any needs of support
for the family.

Patients may often have medical conditions that can preclude them from making capable decisions, ulti-
mately affecting their autonomy. In assessing individual patients, the provider will want to make sure that the
patient can communicate, understand the outlined treatment, reason, and comprehend Withdrawal of Life Support
the risks and benets of accepting treatment. Whether or not an advance directive is present, a patient or their surrogate decision
maker has the right to change their preferences regarding care treatments as their clini-
If the patient is deemed not capable of making his or her own decisions, a surrogate cal condition changes. This allows one to adapt as more information is known. Included
decision maker can be identied to be their voice. Frequently patients do not have a in this are decisions to withhold and withdraw specic medical interventions. It is im-
previously appointed surrogate decision maker. In these cases, relatives are used in the portant to keep in mind that withdrawal of support is not withdrawal of care. Providers
following order (which can vary legally state to state): are still caring for the patient in a different manner. There are often ethical misconcep-
- Spouse (court recognized) tions about withdrawing or withholding medical support, which include patient aban-
- Adult child or majority of adult children available to decide donment, violation of the principle of benecence, or sedatives hastening death. (Table
- Parents 6.2)
- Siblings
- Nearest living relative
Table 6.2: Common Ethical Misconceptions Regarding Foregoing or With-
- Close friends. drawing Support
There can be disputes among relatives as to who is appointed surrogate decision maker.
Alternatively, once a surrogate decision maker is appointed, conict may arise when a Misconception Explanation
treatment plan has been decided. If this is the case, the hospitals ethics committee may Patient Abandonment In reality, the provider continues to care for the patient
be contacted to weigh in on any disagreements that cannot be resolved. with other interventions such as pain control and
psychosocial support to make the transition from one
There are various instruments that help guide treatment based upon the pre-determined intervention to another as comfortable as possible in
wishes of the patient. Advance care planning encompasses a wide range of documents conjunction with patient or family wishes.
whose goal is to outline the patients wishes when the patient is unable to voice them
Violates the principle of For some patients, letting them die in a manner that
during a critical illness. These documents help to guide the surrogate decision maker benecience is consistent with their end-of-life wishes would carry
and health care team about what the patient would or would not have wanted. This may out their best interest. This may mean withdrawing
place less stress and anxiety on those making the decisions. support, even if without this support it may lead to
death sooner.
Under the tenet of advance care planning, these instruments include a health care proxy
or durable power of attorney for health care along with advance directives. A health Administering sedatives or Under the principle of double effect, administering an-
analgesics hastens death algesics for pain control is defensible since the intended
care proxy is a surrogate designated by the patient on a written document who will act of providing relief is the goal of administration. Side
make health care related decisions in the event the patient is unable to do so themself. effects such as respiratory depression and possibly
Advance directives include documents like living wills or instructional directives, which death may occur but are not the intention.
can include specic interventions in the event of certain scenarios such as respiratory
failure or coma. These interventions relate to the patients desire for articial nutrition,
cardiopulmonary resuscitation, ventilator support, invasive surgical measures, etc. The Principle of Double Effect states that an act which may ultimately have undesirable
side effects is permissible if the intended outcome is in itself good, is not intended to do
With advance care planning, the patient and family need to be pro-active and have harm, and outweighs the bad. This is starkly different from physician-assisted suicide
discussions about his or her wishes at the end of life prior to a devastating event. Often, or lethal injection. With few exceptions, the majority of states in the United States
however, patients have not had this conversation and their surrogate decision maker and do not permit physician-assisted suicide. A physician cannot be actively involved in
family are left making informed decisions about what the patient would have wanted. intentionally causing the death of a patient, even if it is in accordance with the patients
This can be an extremely stressful and emotional time for families. The health care team wishes.
needs to anticipate the emotional stress on the families and help them through the dif-
cult process. In the United States, there is no ethical difference between withholding or withdrawing
treatment. It may, however, be hard for families to withdraw life support once it has
been initiated. Over the years, there have been several public court cases about with-
Table 6.1: Principles of Medical Ethics drawal of life-sustaining support such as Karen Ann Quinlan in the 1970s (involving
Principle Explanation withdrawal of ventilator support) and more recently Terri Schiavo in 2005 (involving
withdrawal of nutritional support). These cases among others have set precedence on
Autonomy Patient has the right tho choose or refuse their treatment current ethical standards in the clinical practice.
Benecience Providers deliver care which is in the best interest of the patient
Prior to life sustaining therapy being withdrawn, there are several considerations that
Non-malecence In providing care, do no harm to the patient should be addressed. The family needs to be informed about what to expect, whether
Justice Providing fair care such as allocating resources equally or sys- that be irregular breathing if taken off of the ventilator or a slower wasting if nutritional
tematically among patients

support is withdrawn. It should be emphasized that pain relief will be a primary consid- exam is sufcient. The criteria for brain death can either be made by clinical exam, see
eration and a plan for narcotics or sedatives/anxiolytic agents should be available. below, or in some places it can be made radiographically, i.e. cerebral blood ow exam.
However, according to the 2010 update on determining brain death in adults, there is
In many institutions, there are protocols established to guide withdrawal of life sup- currently insufcient evidence to demonstrate if ancillary tests can accurately determine
port in the most humane way. Ultimately the amount of time until death after support brain death. You need to familiarize yourself with your individual hospital policies and
is withdrawn is difcult to predict. For example, the time to death after withdrawal of state laws. (Table 6.3)
mechanical ventilation usually occurs within 24 hours but can range from minutes to
days or months or, in extreme cases, years. Brain death will cause several pathophysiologic responses and a donor may need to
be supported to maintain perfusion and viability of transplantable organs. This may
Additionally, the family should be prepared emotionally for the dying process. In some include maintaining hemodynamic stability, administering uid, medications or vasoac-
facilities a palliative care service should be involved as emotional and psychological tive agents, and maintaining normothermia. While fatal arrhythmias do occur, systemic
support and aid in the bereavement process. Clergy and social work should also be hypotension is the most common issue in brain death donors. In addition, there is often
involved to provide spiritual and long-term support. Efforts should be made to contact endocrine-hypothalamic-pituitary dysfunction, which may manifest as diabetes insipi-
anyone who would have an interest in seeing the patient prior to withdrawal of life sup- dus, hypoglycemia or hypothermia.
Organ donation after cardiac death involves withdrawal of life-sustaining therapies in
Documentation in the process is also important and a do-not-resuscitate order should be or near the operating room setting. Families may or may not elect to be present at the
completed. This order will detail what is and is not desired by the family in caring for
the patient. This can include the decision to withhold vasoactive medications for blood Table 6.3: Basic Findings to Diagnose Brain Death
pressure support, intubation with mechanical ventilation, or cardiopulmonary resuscita-
tion, specically chest compressions or debrillation. Finding Explanation
Unresponsiveness/Coma Absence of spontaneous or elicited motor
activity (i.e. withdrawal, decorticate or
Organ Donation decerebrate posturing)
Providers in the intensive care unit must be able to recognize prospective organ donors Absence of autonomic response Absence of change in blood pressure or
prior to death. Donated organs can be recovered after the patient meets criteria for heart rate to noxious stimulus in all ex-
brain death or cardiac death. In the United States, over half of the kidneys transplanted tremities (i.e. nail bed pressure)
and the majority of other solid organs (lungs, heart, liver) are obtained from deceased Absence of brainstem reexes No pupillary constriction to light
donors. Legally, organ donation can only be completed when consent is obtained. No oculocephalic reex
No corneal reex with light touch
Once a potential organ donor has been identied, an organ procurement organization No grimacing
(OPO) referral should be made. While hospital policy varies, a referral to the OPO is No gag or cough reex with posterior
usually made prior to withdrawing life support or after meeting criteria for brain death. pharynx stimulation or bronchial suctioning
In accordance with state law variability, disclosure of condential patient information is
allowed per HIPAA to determine eligibility as an organ donor. Apnea Draw an arterial blood gas prior to dis-
connect from ventilator, which must show
The denition of brain death is the irreversible loss of brain functioning. Clinical exam normal pH or normocapnea.
ndings and/or neuroimaging have to support an acute central nervous system catas- Continue monitoring with pulse oximeter,
trophe. Reversible conditions such as electrolyte imbalances, acid-base disorders, drug blood pressure cuff/arterial line, and elec-
intoxication, anesthetic agents, endocrine disturbances, and hypothermia need to be trocardiography.
corrected. Exact limits for core temperature and BP are determined by each state. Ad- Disconnect from ventilator and provide
ditionally, there should be absence of high spinal cord injuries, neuromuscular diseases, oxygen ow through endotracheal tube of
or locked-in syndromes. 4-10 liters/minute.
Repeat arterial blood gas every 5 minutes
while off of ventilator. Test can take as
There are specic diagnostic criteria for brain death and these include unresponsive- long as 15 minutes if there is no respiratory
ness, absence of autonomic reexes, absence of brainstem reexes, and apnea. In the effort, no hypotension (<90 mmHg) or
United States, rules for determining brain death vary by state and individual hospital desaturation (SaO2 <90%).
policy. Typically two separate physicians, usually in the elds of Neurology, Neurosur- Apnea test is positive if:
gery, Internal medicine, Pediatrics, or Anesthesiology, need to agree upon brain death - No respiratory movements
and sometimes these exams must be a designated number of hours apart, i.e 6. The - PaCO2 rises to > 60 mmHg or PaCO2 rises
2010 updated guidelines on determining Brain Death determined there is insufcient >20 mmHg above initial PaCO2
evidence to recommend a minimal observation period and states that one neurologic

time of withdrawal of life support. If the family chooses to be present, life support will
usually be withdrawn in an induction room where the family may say goodbye after Questions
death. A patient is pronounced dead if after ve minutes there is an absence of circula-
tion (pulselessness), along with apnea, unresponsiveness, and asystole on electrocar- 6.1 After you have explained the risks and benets of chemotherapy to a patient recently
diagnosed with leukemia, she has decided not to proceed with chemo and has instead said that
diograph. Once death is certied, the patient is moved to the operating room where she wishes to spend the rest of her days at home with her family. This is an example of which
organ procurement takes place. No organs can be procured until a physician who is not of the four principles of medical ethics?
involved in the transplantation service has certied death. A. Autonomy
B. Benecence
C. Non-malecence
References D. Justice
1. Luce, J.M. and White, D.B: A history of ethics and law in the intensive care unit. Crit
Care Clin 2008; 25(1):221-37. 6.2 A patient has suffered a massive heart attack and is now intubated and on full support
2. Truong, R.D., et al: Recommendations for end-of-life care in the intensive care unit: including a balloon pump. He did not have a living will but who of the following would qualify as
a consensus statement by the American College of Critical Care Medicine. Crit Care Med his surrogate decision maker:
2008; 36(5):1699. A. His mother
3. Mori K., Shingu K, Shinichi N: Brain Death, Millers Anesthesia, 7th Ed. Edited by B. His brother
Miller RD. Orlando, FL: Churchill Livingstone, 2009, pp 3003-30023 C. His best friend
4. Ethics Committee, American College of Critical Care Medicine, Society of Critical Care D. His wife
Medicine. Recommendations for nonheartbeating organ donation: A position paper by the
Ethics Committee, American College of Critical Care Medicine, Society of Critical Care
Medicine. Crit Care Med. 2001; Sep;29(9):1826-31. 6.3 The Principle of Double Effect justies:
5. Wijdicks, Eelco FM, Panayiotis N. Varelas, Gary S. Gronseth, and David M. Greer: A. The practice of euthanasia with the primary goal of hastening death
Evidence-based guideline update: Determining brain death in adults Report of the Qual- B. A provider withholding supportive treatment
ity Standards Subcommittee of the American Academy of Neurology. Neurology, 2010; C. A treatment, which will benet a patient but may have undesirable side effects
74:1911-1918. D. Allocating resources differently among patients

6.4 All of the following are brain stem reexes used in determining brain death except:
A. Oculocephalic reex
B. Corneal reex
C. Gag reex
D. Cervicocollic reex

6.5 The most common complication seen in patients after brain death is:
A. Fatal arrhythmia
B. Hypothermia
C. Hypotension
D. Oliguria

Section 2: Monitoring


Routine Monitoring

Pulse Wave Monitoring

Ultrasound in the ICU

Point of Care Testing

7. Routine Monitoring
Ilya Treskov MD, Thomas J Graetz MD and Brian Wessman MD

Key Points A 78 y/o male with h/o CAD, hypertension, poorly controlled Type
2 Diabetes and COPD is admitted to the ICU for the management of
Continuous hemodynamic monitoring of
respiratory failure and hypotension requiring signicant vasopressor
support. A-line is placed for blood pressure monitoring and frequent arterial
the ICU patients is imperative for the early blood sampling. BP is 100/60.
detection of a worsening disease process and a
timely response to deterioration.

Standard monitors include EKG, pulse

oximetry, blood pressure, temperature as
well as capnography on patients who require
mechanical ventilation.

Rapid interpretation and integration of the

results from the physical exam and various
monitors in the ICU setting as well as the
knowledge of potential pitfalls is essential for
the safe and effective management of critically Blood pressure
ill patients. Manual BP: Indirect measurement of systolic blood pressure (SBP) and diastolic blood pressure (DBP) based
on the auscultation of Korotkoff sounds.

- An appropriately sized BP cuff is inated above SBP and slowly deated
- When the cuff pressure drops below SBP, turbulent ow during systole is auscultated as the rst Korotkoff
- When the cuff pressure drops below DBP, the cuff no longer compresses the artery and the disappearance of
turbulent ow is auscultated as the second Korotkoff sound
- Mean arterial pressure (MAP) is calculated according to the formula
MAP = 1/3 Systolic BP+ 2/3 Diastolic BP

- An inappropriately sized cuff produces erroneous measurements: A cuff too small over-estimates BP; A cuff
to large under-estimates BP.
- BP Cuff width should be about 40% of the limbs circumference. Markings on most BP cuffs conrm
appropriate t.
- BP cuff must be placed at the level of the heart: A cuff too low over-estimates BP; A cuff too high under-
estimates BP (error ~ 0.75 mmHg for every cm above or below the heart)
- Avoid placement of BP cuff on the side of radical mastectomy, PICC line, fast-owing peripheral IV and
- A discrepancy between measurements of BP on different limbs may be caused by Caveats
signicant peripheral vascular disease - Injection of air bubbles or medications into an A-line may lead to limb ischemia and
- The arterial catheter is kept patent by the infusion of uid (3ml/hr) from a pressure
Automatic BP (Oscillometric method): An indirect measurement of SBP and DBP bag; ensure pressure bag remains inated adequately.
based on the detection of oscillations within the BP cuff - BP transducer is generally placed at the level of the heart (or other locations, ex: Circle
of Willis): If the transducer is too low, the measured pressure over-estimates BP; If the
Background: transducer is too high, the measured pressure under-estimates BP.
- BP cuff is inated above SBP and slowly deated. - An artifactual amplication of pressure waves (whip) or dampening of A-line pressure
- The expansions and contractions of the pulsating artery are transmitted to the BP cuff tracing may result in over-estimation and under-estimation of SBP respectively.
and detected as pressure oscillations.
- As the cuff deates, oscillations gradually increase between SBP and MAP and Given the difference in the technique of measuring the manual, oscillometric and inva-
decrease between MAP and DBP. sive BP, some differences between the obtained values are expected. Large disparities
- The point corresponding to maximum amplitude of oscillations approximates MAP. in measurements that impact hemodynamic management, however, need to be meticu-
- SBP and DPB are calculated according to complex, generally proprietary, algorithms. lously investigated to exclude sources of inaccuracy.

Caveats: Pulse Oximetry

- BP cuff size and position (as above) Background:
- Because automatic BP measurement relies on the detection of oscillations, shivering - The pulse oximetry probe utilizes LEDs emitting 2 wavelengths:
and excessive movement may lead to erroneous measurements. 660nm (Red) is predominantly absorbed by Deoxy-Hb
940nm (Infrared) is predominantly absorbed by Oxy-Hb
- Ratio of 660nm/940nm absorbance is the percentage of Hb Saturation
Invasive BP: Direct measurement Since both arterial and venous blood ows under the pulse-ox probe, the computer
calculates arterial Hb saturation by looking for the pulsating, absorbance pattern (thus
Background: pulse-ox). The graph of pulsating absorbance is displayed on the monitor next to the
- SBP and DBP are measured via a pressure transducer connected to an arterial catheter oxygen saturation result (Plethysmographic trace).
with a uid lled, non-compliant tubing. MAP is obtained by calculating the area under
the curve. Caveats:
- In the absence of an adequate plethysmographic trace, the result of pulse ox may be a
The indications for invasive blood pressure monitoring: random number generator!
- Ongoing or anticipated hemodynamic instability - Nail polish (especially blue) may cause inaccuracy in pulse-ox reading
- Requirement of signicant vasopressor support - CO poisoning: Since CO replaces O2 at the same binding site on Hb molecule, the
- Frequent arterial blood sampling absorbance of CarboxyHb and OxyHb at 660nm is the same. Therefore, the pulse ox
- Poorly pulsatile blood ow in patients receiving LVAD or ECMO support will continue to report adequate saturation despite impaired O2 transport.
- Anatomic reasons making other methods of measurement difcult - Methemoglobinemia: Pulse-ox is about 85% with little response to supplemental O2 .
List of potential causes is very long! Note:
Location: - Benzocaine (ingredient of Cetacaine spray)
- Most common: Radial artery - Prilocaine (ingredient of EMLA cream)
i. Advantages: supercial anatomical location, relative distance from large veins and - Nitric Oxide, Nitroglycerin, Sodium Nitroprusside
nerves as well as considerable collateral circulation - Acetaminophen overdose
ii. Disadvantages: Relatively small arterial diameter means the catheter occupies a - An injection of dyes such as methylene blue and indigo carmine produces spuriously
signicant portion of the intraluminal space, impeding the ow and increasing the risk low readings
of arterial thrombosis (risk of thrombosis with 18g is increased relative to 20g catheter); - An intense ambient light may interfere with pulse-ox. Cover pulse ox probe to
a modied Allans test may be utilized to assess collateral circulation although its utility improve plethysmographic trace.
is disputed. - Since pulse ox is looking for pulsating pattern of light absorption, motion artifact (ex:
- Alternatives: Femoral, axillary, brachial, temporal and dorsalis pedis arteries. shivering) is a potential source of inaccuracy
- As the arterial line is placed more peripherally, the systolic pressure will be greater and
the diastolic pressure slightly lower. The MAP will be the same no matter where the The integration of information from various monitors may help recognize artifactual
pressure is measured. readings: If the EKG shows disorganized activity but A-line demonstrates regular pulse,
- In patients with VA ECMO (particularly peripheral ECMO), the A-line is preferentially EKG artifact is most likely.
placed in the right radial artery to allow for sampling of the arterial blood that reects
oxygen saturation supplied to the brain
- ICU monitors typically analyze 7 leads: I, II, III, AVF, AVL, AVR and V5
- Placement mnemonic: smoke (black) over re (red); brown - V5 (5th intercostal space
mid-axillary line); white is right; snow (white) on the grass (green)
- V5 is most sensitive to ischemia (followed by V4).
- Lead II is most sensitive to arrhythmia.
- For precise EKG interpretation, get a 12 lead EKG.

- Rate: Bradycardia <60bpm; Tachycardia > 100bpm
- Rhythm:
Regular or Irregular?
P waves before each QRS?
Wide or narrow complex? Normal QRS < 120ms
Conduction block? Normal PR < 200ms
QT interval (prolonged by a variety of drugs) and corrected for heart rate; Normal
QTc < 450ms in males and <470ms in females Figure 7.1 Capnogram
- Axis: 0 - Phase 0 (Inspiration); I - Phase I (Anatomical and apparatus dead space); II - Phase
I and AVF are positive, axis is normal (2 thumbs up!) II (Mixture of dead space and alveolar gas); III - Phase III (Alveolar plateau)
I AVF extreme right axis deviation.
I AVF right axis deviation - Morphology of capnometry waves
I AVF left axis deviation (if lead II is negative) Bronchospasm
- Ischemia: ETT tube occlusion
1 mm ST-segment depression or T-wave inversion ischemia - Detection of esophageal intubation
1 mm ST segment elevation in 2 contiguous leads acute MI
Interpretation of ETCO2 numerical value:
- Normal 35 45 mmHg
Temperature - Decrease in ETCO2:
Background: Ventilation causes:
- Core temperature (PA catheter, tympanic membrane, bladder, rectal, esophageal) - Hyperventilation
- Surface temperature (skin, oral) Circulation causes:
- Pulmonary embolism
Hypothermia - Decreased cardiac output
- Leads to confusion, delirium, delayed awakening from anesthesia. - Minimal or absent ETCO2:
- Shivering increases O2 demand. Equipment causes:
- ETCO2 sample line occlusion
Fever Ventilation causes:
- Greater than 42C is associated with dysfunction of endogenous enzymes and multi- - Apnea
organ failure. Patient may require active cooling. - ETT occlusion
- Is deleterious in patients with ischemic, hemorrhagic or traumatic brain injury, post- - Esophageal intubation
cardiac arrest. - Bilateral pneumothorax
Circulation causes:
- Catastrophic cardiovascular collapse
Capnometry - Massive PE
Background: - Increase in ETCO2:
- Measurement and graphical representation of partial pressure of CO2 (ETCO2) in Increase in metabolism/ production of CO2:
expired gas - Administration of Sodium Bicarbonate
- Hyper-metabolic state (sepsis, hyperthyroidism)
Applications: (Figure 7.1) Decrease in elimination:
- Conrmation of endotracheal intubation - Hypoventilation
- Assessment of cardiac output

ventricular (RV) contraction.
In a code situation: - x-descent: RA relaxation and downward displacement of the TV during systole
- Conrmation of chest compression effectiveness (goal: ETCO2 10-20mmHg) - v wave: Venous lling of RA against closed tricuspid valve, generally immediately
- Detection of the return of spontaneous circulation (sudden rise in ETCO2) after peak of T wave on EKG
- y-descent: Emptying of RA upon opening of the tricuspid valve (diastolic lling)
Background: Abnormal CVP waveforms:
- Measurement of venous blood pressure at the superior vena cava (SVC) right atrium - Atrial Fibrillation: obliteration of the a wave, prominent c wave
(RA) junction - Complete AV block: Cannon a waves
- Normal CVP ~5-10 cmH2O

A careful analysis of the CVP trace may aid in diagnosis of a variety of pathological References:
condition including atrial brillation, complete AV block, tricuspid valve regurgitation 1. Barash PG, Cullen BF, Stoelting RK: Clinical Anesthesia, 6th edition. Philadelphia,
Lippincott-Raven Publishers; 2009, pp 697-715
and stenosis. 2. Miller MD, Ronald D., Eriksson, Lars I., Fleisher MD, Lee, W: Cardiovascular Monitor-
ing, Millers Anesthesia, 7th ed. Churchill Livingstone, 2009, pp 1267-1328.
3. Butterworth IV JF, Mackey DC, Wasnick JD: Cardiovascular Monitoring, Morgan &
Mikhails Clinical Anesthesiology, 5e. The McGraw-Hill Companies, Inc, 2013, pp 87-122.
4. Deborah J. Cook D, Simel D: Does This Patient Have Abnormal Central Venous Pres-
sure? JAMA 1996; 275:630-4
5. Bhavani-Shankar K, Moseley H, Kumar AY, Delph Y: Capnometry and anaesthesia.
Can J Anaesth 1992; 39:617-32
6. Website:; Pulse oximetry tutorial: http://www.howequip-

7.1 A-line is placed for blood pressure monitoring and frequent arterial blood sampling. BP is
100/60. If the arterial line transducer was accidentally lowered by 80cm, what pressure will be
displayed on the monitor?
A. 180/140 mmHg
B. 160/120 mmHg
C. 100/60 mmHg
D. 60/40 mmHg

7.2 What EKG lead is most sensitive to ischemia?

A. V5
B. V4

7.3 A patient suffers a sudden cardiac arrest and CPR is initiated. What is the best measure of
Figure 7.2 CVP Waveforms the effectiveness of chest compressions?
A: Normal EKG; B: Normal CVP tracing; C: CVP tracing in atrial brillation; A. O2 saturation
D: CVP tracing with cannon a-wave, where atrial contraction occurs against a B. BP
closed tricuspid valve C. ETCO2
D. pH

CVP waveform: (Figure 7.2)

- a wave: An increase in the venous pressure caused by the right atrial (RA) contraction
- c wave: Motion of the tricuspid valve (TV) toward the RA during early right

8. Pulse Wave Monitoring
Aalok Kacha MD PhD

Key Points You are taking care of a 57-year-old man with end-stage liver disease,
now newly post-op orthotopic liver transplantation. In the ICU, his heart
The adequacy of cardiac output should be
rate is 90/minute with a blood pressure of 90/50 mmHg with a declining
urine output. He remains intubated on cisatracurium, propofol, and
based on individual patient assessment norepinephrine infusions. There are multiple invasive monitors in place
including a pulmonary artery catheter and an arterial line. His chest X-ray
Static pressure measurements such as is concerning for an alveolar lling process and you are unsure whether his
CVP and PCWP are not an accurate way to declining urine output is best managed with administration of additional IV
determine whether a patient is fluid responsive uid or diuretic medications.

PPV and SPV are useful tools to guide fluid

therapy in patients who meet criteria for their

Arterial pressure monitoring

Invasive arterial monitoring is frequently used to measure blood pressure and for serial arterial blood gas
analysis. An arterial catheter is connected to rigid uid-lled tubing of a monitoring system. The uid column
in the tubing carries a mechanical signal created by the arterial pressure wave to the diaphragm of an electri-
cal pressure transducer that converts the mechanical signal into an electrical signal. The electrical signal is
transmitted to the monitor and then is amplied and displayed.

In order to assess the accuracy of the arterial pressure waveform, a fast-ush test is used. A brief ush can
be applied to the catheter tubing system to determine whether the recording system is distorting the pressure
waveform or not. Most systems are equipped with a one-way valve that can be used to deliver a ush from a
pressurized uid bag (usually at 300 mmHg). This ush causes the pressure to increase rapidly with a square
wave tracing. Release of the ush should result in a return to baseline after several oscillations. An optimally
functioning system has one undershoot and a small overshoot before returning to baseline. An overdamped
waveform may be due to the presence of bubbles, clot, lack of ush solution, lack of pressure in the ush
system, or excessive bends in the system tubing. Underdamping is usually due to excessive tubing length (>
200 cm) or the use of excessively stiff tubing.

As the pulse travels from the aorta to the periphery, the systolic pressure is amplied by reected waves from
the periphery. This pulse amplication results in distal measurements (e.g., radial artery) having a greater
systolic pressure and slightly lower diastolic pressure compared to more proximal measurements (e.g., the
femoral artery). The initial upswing (dP/dT) of the arterial waveform is called the anacrotic limb and changes
with cardiac contractility. It is steeper with the use of inotropes and shallower when decreased left ventricular afterload. This increased stroke volume results in an inspira-
contractility is impaired. The dicrotic notch signies aortic valve closure. tory increase in systolic blood pressure and a greater pulse pressure (smaller effect on
diastolic pressure). Subsequent stroke volumes will decrease, reecting the previously
Clinical assessment for uid administration decreased venous return to the right ventricle. These smaller stroke volumes will result
The need to assess the intravascular volume status of a patient is commonplace in the in a delayed (after the positive pressure breath is delivered) decrease in systolic blood
intensive care unit and operating room. This is often prompted by clinical scenarios pressure and a smaller pulse pressure. For animated slides illustrating the intersection
such as low urine output, low blood pressure, or high heart rate, suggesting that intra- of the venous return and Starling curves, please refer to the supplemental material from
venous uid therapy may be warranted. Other information such as chest auscultation, Magder, 2004.
chest radiograph, examination of mucous membranes, or skin turgor has been used to
guide clinical decision-making regarding uid therapy. In addition to these clinical as- The dynamic changes in the interaction between venous return and cardiac function that
sessments, invasive monitoring of lling pressures has been traditionally used to guide occur with ventilation can be used clinically. The effects of the varying stroke volumes
uid therapy in the intensive care unit and operating room. on beat-to-beat systolic blood pressure and pulse pressure can be observed in patients
with an arterial line. Unlike static measures such as CVP and PCWP, the dynamic
The most commonly used of these is central venous pressure (CVP), which is read- indices of pulse pressure variation (PPV) and systolic pressure variation (SPV) de-
ily assessed by transduction of a central venous catheter. The use of CVP monitoring rived from pulse contour analysis have been demonstrated to be a useful guide to uid
is predicated on the assumption that this measurement reects right ventricular pre- therapy. Although the focus will be on PPV as it is most convenient index to obtain with
load. The assessment of left ventricular preload has traditionally been estimated by an automatic calculations by modern day monitoring equipment, SPV is readily accessible
analogous measurement of the pulmonary capillary wedge pressure (PCWP) obtained by examination of the arterial line. Since these phenomena are tied to changes in pleural
after placement of a pulmonary artery catheter. These pressure measurements of cardiac pressure, they do occur in spontaneously ventilating patients as well, but their use in
lling pressures have not been shown to be an effective tool for guiding uid therapy. It patients breathing spontaneously has not been completely validated.
is likely that this failure reects the static nature of the measurements as an attempt to
estimate preload or blood volume rather than dynamically determining the response to a
uid challenge. Application of PPV
In patients who are uid responsive, the intersection of the venous return and cardiac
In the clinical scenarios in which one is considering uid therapy and wants to assess function curves is such that patients are on the steep portion of the Frank-Starling curve
intravascular uid status, the question that needs to be answered is whether there will be (Figure 8.1). This leads to larger changes in stroke volume, SPV, and PPV with mechan-
a clinically signicant increase in cardiac output if uids are administered. This ques- ical ventilation as compared to patients in whom the intersection of the venous return
tion can be answered using the normal changes in stroke volume and cardiac output that and cardiac function curves occurs on the at portion of the Starling curve (and who are
occur with positive pressure mechanical ventilation. not uid responsive).

The use of PPV to guide uid

Physiologic basis of pulse pressure variation and systolic therapy has been best characterized
pressure variation in patients with a controlled set of
The stroke volume varies throughout the respiratory cycle due to the interaction variables. This tool is most useful
between venous return and cardiac function. Changes in pleural pressure affects the when all of the following conditions
circulation by changing right and left ventricular loading and the pressure relationship are met.
between intrathoracic and extrathoracic structures. Properly functioning arterial line
and measurement system
During positive pressure inspiration, a decrease in vena caval ow is followed by Regular cardiac rhythm without
decreases in pulmonary arterial ow and aortic ow. The initial decrease in venous arrhythmias or extra-systoles
return is likely to due to transmission of the increased pleural pressure to intrathoracic Mechanical ventilation with tidal
structures causing an increased right atrial pressure (hindering venous return) and com- volumes of 8 mL/kg
pression of the intrathoracic vena cava. This decrease in venous return, via the Frank- Passive interaction between patient
Starling relationship, results in a decrease in right-sided cardiac output that results in a and ventilator without triggered
delayed (due to the pulmonary transit time of approximately 2 seconds) decrease in left breaths or dyssynchrony
ventricular preload and cardiac output. The left ventricle is also affected by inspiration:
the positive pleural pressure decreases the transmural pressure required to eject blood Figure 8.1 Frank Starling curve applied to PPV Pulse pressure variation (Figure 8.2)
into the aorta and thus effectively decreases left ventricular afterload. is calculated as a percentage based
on the greatest and least pulse pressures measured during a respiratory cycle:
In summary, with the delivery of a positive pressure breath, there is a decrease in PPV = 100 x (PPmax PPmin)/[(PPmax + PPmin)/2].
venous return to the right ventricle and a decrease in the afterload of the left ventricle. In contrast, SPV is assessed using the end expiratory apneic systolic blood pressure as
These produce an increase in stroke volume during inspiration, due to the effect of the the baseline. With positive pressure ventilation, an increase in the systolic pressure is

referred to as delta up and a decrease as delta down (which correlates best with preload siveness? A systematic review of the literature and the tale of seven mares. Chest 2008;
dependence and uid responsiveness). 134:172-8
4. Marik PE, Cavallazzi R, Vasu T, Hirani A: Dynamic changes in arterial waveform de-
rived variables and uid responsiveness in mechanically ventilated patients: a systematic
Although precise thresholds for the use of the PPV to determine uid responsiveness review of the literature. Crit Care Med 2009; 37:2642-7
vary, a PPV < 10% suggests that the patient will not be uid responsive while a PPV > 5. Michard F: Changes in arterial pressure during mechanical ventilation. Anesthesiol-
15% suggests that the patient will be uid responsive. These values can be used to guide ogy 2005; 103:419-28
uid therapy, but consideration must be given to the clinical condition of the patient and
the details of the clinical scenario, as differences in physiology may affect the interac-
tion between the ventilator and cardiac output in any particular patient.

There are multiple limitations to the use of PPV that should be considered when using
this tool.
Malfunctioning arterial line and measurement system
Irregular cardiac rhythm or frequent extra-systoles
Mechanical ventilation with small tidal volumes (<8 ml/kg)
Patient-ventilator dyssynchrony or spontaneous breathing
Open-chest conditions
Presence of right ventricular failure or pulmonary hypertension

8.1 A poor dP/dT on the arterial waveform would favor selection of which of the following

A. Vasopressin
B. Furosemide
C. Phenylephrine
D. Dobutamine

8.2 Of the following, which is the best to determine uid responsiveness?

D. Left ventricular end-diastolic area index

8.3 In a hypotensive patient with a normal cardiac function, which of the following could indicate
Figure 8.2 Pulse-Pressure Variation the need for uid therapy?
Changes seen during a single respiratory cycle.
A. CVP 6 cm H2O
B. PPV > 15%
C. PCWP 10 cm H2O
D. PPV < 10%
This chapter is a revision of the original chapter authored by Lalitha Sundararaman, M.D.
8.4 The delta down on the systolic pressure variation reects:

References A. Preload
1. Jacobsohn E, Chorn R, OConnor M: The role of the vasculature in regulating ve- B. Afterload dependence
nous return and cardiac output: historical and graphical approach. Can J Anaesth 1997; C. Contractility
44:849-67 D. Diastolic dysfunction
2. Magder S: Clinical usefulness of respiratory variations in arterial pressure. Am J
Respir Crit Care Med 2004; 169:151-5
3. Marik PE, Baram M, Vahid B: Does central venous pressure predict uid respon-

9. Ultrasound
Rohit Patel MD

Key Points A 59 year old obese male with a history of pulmonary hypertension arrives
to the intensive care unit after coronary artery bypass grafting and mitral
Point of care ultrasound has been shown
and aortic valve replacement. The patient is intubated and receiving
therapy with norepinephrine and epinephrine infusions but continues to
to make an impact on decision making and be hemodynamically unstable with a heart rate of 123, blood pressure of
improve patient outcomes 83/58, and oxygen saturation of 92% on 100% oxygen. Central venous
pressure is estimated at 16 and pulmonary pressures are estimated at
Lung ultrasound has had increased use 57/34 with a pulmonary artery occlusion pressure of 23.
over the past ten years and continues to have
evidence base for use in the critically ill patient

Reproducibility is probably one of the most

important aspects of point of care critical care

Ultrasonography use is becoming an indispensable tool in the practice of critical care medicine. Its safety and
portability allow for rapid noninvasive bedside assessment to aid in diagnosis and ongoing management of
critically ill patients. In particular the etiology of hemodynamic instability can be difcult to ascertain in pa-
tients with cardiac pathophysiology without the use of this diagnostic tool. Other ultrasound modalities useful
in the intensive care unit are vascular ultrasound (for access and evaluation of thrombosis), abdominal ultra-
sound (for evaluation of free uid, aorta pathology), lung ultrasound (for evaluation of pleura, pneumothorax,
interstitial edema, pleural effusion, and consolidations including pneumonia or atelectasis). The American
College of Chest Physicians and Society of Critical Care Medicine have made recommendations on critical
care ultrasound competencies1,2. Resuscitation efforts are frequently redirected based on ultrasound ndings.
Also it has been shown in recent literature that ultrasound has a high impact on management decisions made
in the intensive care unit3. Lung ultrasound also has made great advances over the past 10 years and has
become more useful in the evaluation of the acute hypoxic patient4, 5.

Both transthoracic and transesophageal echocardiography can be used to evaluate cardiovascular compromise.
Various protocols have been developed in evaluation of the acute hypotensive patient (RUSH, FATE, FEEL,
CAUSE, etc), but more importantly it is critical to remember to use the ndings and the appropriate clinical
setting to make the decision. As the clinician taking care of the patient and the operator of ultrasound image
acquisition, the clinician has the advantage of making immediate decisions and impact on patient care. Ultra-
sound in the ICU has changed from organ specic evaluation to problem based evaluation. A prime example
of this is how abdominal evaluation in trauma has been renamed from FAST (Focused Abdominal Sonog-
raphy in Trauma) to FAST (Focused Assessment with Sonography in Trauma), which c) Unexplained Hypoxemia
shows a change from focus of organ (abdomen) to focus of problem (trauma). d) Sources of Emboli
3. Chest Trauma with Hemodynamic Compromise
The case presentation illustrates the difculty that can be encountered when treating B. Indications for TEE over TTE - High image quality is vital
hemodynamic instability. Despite both epinephrine and norepinephrine infusions the pa- 1. Aortic Dissection
tient continues to exhibit a poor hemodynamic status. Although central venous and pul- 2. Endocarditis
monary catheter data are available, the diagnosis remains elusive. The clinical picture 3. Intracardiac Thrombus
is consistent with left ventricular failure but is also compatible with right heart failure, 4. Structures that may be inadequately seen on TTE
valvular dysfunction or cardiac tamponade. Echocardiography can provide real time a) Thoracic Aorta
images to distinguish between these etiologies. b) LA Appendage
c) Prosthetic Valves
Ultrasonography, particularly echocardiography, requires a formal education. The out- 5. Patient conditions that prevent image clarity on TTE
line below simply aims to provide a basic understanding of the use of ultrasonography a) Severe Obesity
in the critically ill patient and therefore cannot substitute for formal training in critical b) Emphysema
care ultrasound1,2. c) High PEEP
d) Surgical drains, Incisions, Dressings
More information is available online from the authors fellowship education curriculum C. TEE Complications
site at 1. Odynophagia: 0.1%
2. Dental Injury: 0.03%
Didactics ( 3. Endotracheal Tube Dislodgment: 0.03%
the following are applications and particular situations where they may be useful. Refer 4. Esophageal Perforation: 0.01%
to more comprehensive resources on each individual topic listed. D. Contraindications to TEE
1. Absolute
Examinations a) Esophageal Stricture
b) Esophageal Mass
c) Esophageal Diverticulum
d) Mallory-Weiss Tear
e) Dysphagia/Odynophagia Unevaluated
f) Cervical Spine Instability
2. Relative
a) Esophageal Varices
b) Recent Esophageal/gastric Surgery
c) Oropharyngeal Carcinoma
d) Upper GI Bleeding
e) Severe Cervical Arthritis
f) Atlantoaxial Disease
E. Echocardiography ndings in hemodynamic instability (LV function best assessed
at the parasternal short papillary muscle level) - hypovolemic, cardiogenic, obstructive
Figure 9.1 Pericardial Effusion: This patient with shortness of breath and chest pain shock all have specic ndings.
shows evidence of diastolic collapse of the right ventricle. F. Hypovolemic Shock
1. Decreased End-Diastolic Area
Cardiac 2. Kissing Papillary Muscle
A. Indications 3. Hyperdynamic Function
1. Hemodynamic Instability G. Cardiogenic Shock
a) Ventricular Failure 1. Failing Left Ventricle
b) Hypovolemia a) Decreased Area Change
c) Pulmonary Embolism b) Increased End-Diastolic Area
d) Acute Valvular Dysfunction c) Increased End Systolic Area
e) Cardiac Tamponade 2. Failing Right Ventricle
2. Complications after Cardiothoracic Surgery a) Increased Right Ventricular Size
a) Infective Endocarditis b) Intraventricular Septum bulges towards Left Ventricle
b) Suspected Aortic Dissection or Rupture c) Pulmonary Embolus if echogenic density present
3. Valvular Pathology
a) Mitral Regurgitation pneumonia
b) Mitral Stenosis 3. Identication of Pulmonary Edema (Interstitial syndrome) - B lines with lung
c) Aortic Regurgitation sliding found in anterior lung zones
d) Aortic Stenosis
4. Cardiac Tamponade Vascular
a) Pericardial Effusion A. Identication of Deep Vein Thrombosis - non-compressible vein
b) Diastolic Collapse of Right Ventricle B. Vascular Access (central vein, artery, hemodialysis): Dynamic guidance is when the
procedure is performed under direct guidance, with real time view of the needle. Other
methods of use include blind and semi-blind techniques.

Figure 9.3 CVP Placement: Long and short axis views conrm placement of wire prior
to placing CVP catheter in typical ICU patient.

A. Identication, Quantication and Characterization of Intraperitoneal Fluid. This is
done routinely during the FAST (Focused Assessment with Sonography for Trauma)
Figure 9.2 Lung exam: Anterior chest B lines are seen in a patient with hemodynamic exam in the evaluation of the trauma patient.
pulmonary edema initially suspected to be COPD. Based on this ultrasound, the pa- Areas investigated include hepatorenal, splenorenal, pericardial space, and bladder
tient was given diuretics and/or afterload reducing agents to treat the acute exacerba- (posterior to bladder for uid).
tion of CHF with a BP 200/100.
B.Assessment of Urinary Tract
Lung b)Distended Bladder (ureteral jets)
A. Pleural C. Identication of Abdominal Aortic Aneurysm and Dissection
1. Pneumothorax Identication - absence of lung sliding, and lung point which
you can see part of the pleura sliding and the other part absent sliding, indicates
pneumothorax and can estimate size based on location Tip sheets for all the above modalities can be found at:
2. Effusion Identication, Characterization and Quantication - quad and sinusoid tion/ultrasound/tip-sheets/
signs, anechoic space between diaphragm and lung. This can be used to estimate size,
and lung pathology
3. Guidance during Thoracentesis - can use vascular probe to visualize rib space in
obese patients, as well as best approach
B. Lung
1. Identication of Aerated Normal Lung - in respiratory failure patients can signify
obstructive lung disease (COPD, asthma) or pulmonary embolism - A lines which are
horizontal lines and represent reverberation artifacts of the pleural line
2. Identication of Consolidated Lung with or without Air Bronchograms - can use to
differentiate atelectasis from pneumonia - B lines without lung sliding can indicate
Figure 9.4 FAST Exam for Trauma: Free uid is seen in this trauma patient with hypo-
tension. There was no obvious cause of bleeding. The patient was found to have a
liver laceration on laparotomy.

Ultrasonography provides the critical care physician with a tool to rapidly assess a pa-
tients condition. It is safe and can be used at the patients bedside. The most important
quality of bedside/portable/point of care ultrasound is reproducibility. As the clini-
cian taking care of the patient, you can make interventions and immediately evaluate
to see the results of your intervention. With technological advances image quality has
improved allowing for the development of new applications for ultrasonography. As
experience with this diagnostic modality has increased it is clear that ultrasound use will
become ubiquitous with the practice of critical care medicine.

1. Mayo P, Beaulieu Y, Doelken P, et al: American College of Chest Physicians/La Societe
de Reanimation de Langue Francaise Statement on Competence in Critical Care Ultraso-
nography. Chest 2009; 135:1050-60.
2. Neri L; Storti E; Lichtenstein D: Toward an ultrasound curriculum for critical care
medicine. Crit Care Med 2007; 35:S290-S304
3. Manno E, Navarra M, et al: Deep Impact of Ultrasound in the Intensive Care Unit:
The ICU-sound protocol. Anesthesiology 2012; 117:801-809
4. Volpicelli G, et al: International evidence-based recommendations for point-of-care
lung ultrasound. Intensive Care Med 2012; 38: 577-591
5. Lichtenstein D, Meziere G: Relevance of Lung Ultrasound in the Diagnosis of Acute
Respiratory Failure: The BLUE protocol. Chest 2008; 134: 117-125.
6. Noble V, Nelson B, Sutingco A: Manual Emergency and Critical Care Ultrasound. New
York, Cambridge University Press, 2007.
7. Beaulieu Y, Marik P: Bedside Ultrasonography in the ICU Part 1. Chest 2005;
8. Beaulieu Y, Marik P. Bedside Ultrasonography in the ICU Part 2. Chest 2005;

Questions 9.4 A middle-aged man is a victim of a stab wound to the chest. He is hypotensive. A bedside
TTE is performed and the image below is obtained. What is located by the area indicated by the
9.1 Which of the following is not evaluated during a typical FAST exam?
A. Pericardial space
B. Hepatorenal space
C. Splenorenal space
D. Aorta

9.2 Dynamic approach for line insertion using ultrasound means:

A. The procedure is done blindly but after having localized the vein prior to procedure
B. The procedure is done with ultrasound in the Doppler mode to see the dynamic blood
C. The procedure is done with ultrasound after the blind approach fails
D. The procedure is performed under direct guidance, with real time view of the needle

9.3 Which pulmonary pathology is ultrasound unable to assess?

A. Pneumothorax
B. Pulmonary Edema
C. Pulmonary Embolism
D. Pneumonia
E. Ultrasound is able to aid in diagnosis of all of these etiologies

A. Left Ventricle
B. Right Ventricle
C. Lung
D. Pericardial effusion
E. Liver

10. Point of Care Testing in the ICU
Rebecca Kalman MD and Edward A Bittner MD PhD

Key Points A 72 year-old man was transferred to the ICU from the oor for an
increasing oxygen requirement and an altered mental status. He was
Point-of-care testing (POCT) refers to testing
admitted to the hospital two days prior for diverticulitis and has a medical
history signicant for insulin dependent diabetes, coronary artery disease,
performed at or near the patients bedside, and prior stroke. Shortly after arrival to the ICU, his condition worsened
outside of the confines of a centralized clinical and he became hypotensive and unresponsive. He was resuscitated with IV
laboratory, and has been shown to reduce the uids and intubated. Blood was drawn for analysis and an upright KUB was
therapeutic turn-around time (TTAT). obtained. The KUB revealed free air and he was rushed to the operating
room. Twenty minutes after he left the ICU, the laboratory called to report
The institution of POCT involves staff a critical value. The glucose was 26 mg/dL. Would knowledge of this value
education in appropriate device use, device have changed his management?
maintenance, and device quality control. It
does not necessarily correlate to improvements
in clinical outcome.

POCT is available for many laboratory tests

commonly obtained in the ICU including
glucose, blood gas, electrolytes, lactate, and Introduction
coagulation studies. In taking care of critically ill patients, the time to diagnosis and treatment of life threatening issues can be
crucial. Traditionally, most laboratory tests ordered are performed off the unit in a central or STAT laboratory.
This involves a multistep process in which tests are ordered, samples are drawn, labeled, and transported to
POCT is more likely to be of benefit in the laboratory. There, they are analyzed and the results then communicated back to the requesting unit/physi-
situations where patients clinical condition cian (Figure 10.1).1 These processes take time and the time interval between laboratory test order to treat-
changes rapidly or when laboratory values ment decision is referred to as the therapeutic turnaround time (TTAT). In the ICU, the clinical condition of
need to be obtained quickly. unstable patients can change quickly and rapid turnaround in laboratory tests is required for prompt diagnosis,
early therapy, and changes in management. Consequently, delays causing an increase in TTAT may have
detrimental effects.

Point-of-care test(ing), commonly referred to as POCT, is testing performed at or near the patients bedside,
outside of the connes of a centralized clinical laboratory. POCT is usually performed on whole blood with
user-friendly devices located either directly at the patients bedside or within the ICU. Studies have shown
that POCT, when compared to central laboratory testing, reduces TTAT.2,3 In one randomized, controlled trial
performed in an emergency department, patients blood was randomly allocated to POCT versus testing by
the hospitals central laboratory. In the POCT group, there was a reduction in TTAT and overall time needed
to make decisions regarding patient management. In addition, time to treatment was reduced for patients with
conditions where timing was considered to be critical. However, these changes did not affect clinical out-
hypoglycemia, bedside glucometers are the standard in many ICUs. However, glucose
Advantages and Disadvantages of POCT values obtained with a point-of-care device can differ signicantly from those obtained
by laboratory analysis. Laboratory or plasma glucose levels are usually higher than
One of the biggest advantages of POCT is in the reduction of TTAT leading to rapid whole blood POCT results due to differing ratios of water content in the samples. For
data availability, and faster real-time patient management and clinical decision-making. this reason, a calibration factor is incorporated into POCT devices. In addition, values
There is, also, a decreased chance for errors associated with specimen handling, label- drawn from a central venous catheter can differ from those obtained from a nger stick.
ing, and transport. Most POCT require smaller blood volumes, thus decreasing iatro- Other factors affecting the accuracy of POCT glucose results include a patients hemato-
genic blood loss. In addition, POCT is often cost saving. crit and enzyme degradation of testing strips. 5

Potential disadvantages of POCT include less consistent sample handling, poor analytic BLOOD GAS
performance, unauthorized testing, potential for transcription, communication, and Oxygenation, ventilation, and acid-base status are of major concern in the critically
documentation lapses due to less formal protocols, inadequate training of personnel per- ill patient. Life threatening changes in these parameters can occur suddenly and rapid
forming the test, validation error of test results, limited test menu, and lack of a notica- results are often key to diagnosis and treatment. POCT has the potential to decrease
tion system or documentation for critical values. TTAT for these crucial values. Blood gas testing has been mentioned as the most-often
needed POCT in the ICU. In fact, there is some evidence that POC blood gas testing
POCT devices and tests leads to improved clinical outcomes when there is a reduction in TTAT. However, these
results were not consistent across all studies. For example, in a report of one centers
experience with POCT for blood gas analysis, inaccuracies in pCO2 measurements were
identied that eventually led to the discontinuation of the POCT. It was eventually
determined that the discrepancies were due to incompatibility between testing syringes
and the device, illustrating the complexity of implementing POCT in the critical care

In the ICU, many conditions can lead to electrolyte abnormalities and these can be
life-threatening if not detected and treated. When a microanalyzer was implemented
to analyze electrolytes and blood gases, on trauma patients in the emergency room, the
reported laboratory values were accurate and fast and provided more information for
evaluation and management of the patient. They were specically found to be help-
ful in patients requiring urgent or emergent operative intervention as laboratory data
obtained via POCT were more likely to be available pre-operatively.7

Recognizing an elevated lactate level leads to the diagnosis and treatment of tissue
Figure 10.1 Different steps in testing with POC vs Central Laboratory hypo-perfusion whether it be related to sepsis, vascular ischemia, or hemorrhage. The
use of lactate POCT has been reported to improve mortality in neonates and other high-
There are a variety of POCT devices and tests. Most POCT devices require blood to be risk patients undergoing congenital heart surgery.8
drawn from the patient, similar to samples sent to the lab. However, some POCT can be
performed in vivo allowing testing on whole blood without removing it from the body. COAGULATION STUDIES
An example is the use of beroptic pulmonary artery catheters to continuously measure Critically ill patients may have disorders of coagulation related to their underlying
mixed venous oxygen saturation (SvO2). Other in vivo tests include subcutaneous real- illness, hemorrhage, uid administration, or medications. Timely evaluation of coagu-
time glucose monitoring or measurement of arterial blood gas via intra-arterial sensors.1 lation status can facilitate appropriate use of blood products and related medications.
Traditional methods of monitoring coagulation, including the prothrombin time (PT),
Specic situations in which POCT may be helpful in the ICU include the monitoring of activated partial thromboplastin time (aPTT), international normalized ratio (INR),
glucose, electrolytes, blood gas, lactate, and coagulation studies. They are described in platelet count, and brinogen levels, may be time consuming to obtain and do not fully
more detail below. characterize the risk of bleeding.

GLUCOSE Activated clotting time (ACT) is a common POCT used to evaluate the intrinsic or com-
Glucose control is an integral part of ICU care as both hyper- and hypoglycemia are mon pathway of coagulation. A whole blood sample is added to an activator (diatoma-
associated with increased morbidity and mortality.4 Critically ill patients can have ceous earth or clay) and the time to clot formation is measured. It is often used in the
large uctuations in blood glucose levels inuenced by stress, medications, and co-
morbidities. Given that there are time dependent risks associated with both hyper- and

operating room when monitoring the effect of heparin therapy or anticoagulation by Since POCT generates information leading to clinical decisions, it is essential to ensure
direct thrombin inhibitors such as argatroban, bivalirudin, and lepirudin. a proper quality management program overseeing its use. A close, ongoing relationship
with the central laboratory is key since many characteristics of POCT must be checked
Thromboelastography (TEG) is a POCT method that evaluates multiple levels of the and continuously monitored by the laboratory including the choice of methods, initial
coagulation cascade. It measures the movement of a pin placed in a rotating cup lled and ongoing staff training, proper equipment maintenance, and management of consum-
with whole blood mixed with kaolin. As clot forms, the freely hanging pin becomes ables. An internal quality control program performed at least once daily with monthly
bound to the rotating cup and movement of the pin is recorded to produce a graph with reviews of performance as well as periodic quality assessment of each instrument and
parameters (Figure 10.2). TEG has been reported to accurately predict peri-operative appropriate procedures for recording results are other essential components of a POCT
and post-operative bleeding and can have value in targeting coagulation treatment. (9) quality assurance program.
Its use has also been associated with a decrease in blood product use after elective coro-
nary artery bypass grafting.10 Precise sample handling and aliquot transfer is important
to ensure accurate TEG measurements. In addition, evaluation of platelet function can
be inaccurate in the presence of platelet inhibitors.11
There are several POCT devices available for the testing of platelet function. Some
1. Gupta S, Bhattacharya A. Point of Care Testing in anaesthesiology and intensive care
devices provide standard complete blood counts, including platelet count and evaluation An overview. Indian J Anaesth 2004;48(4):278-86
of platelet function such as aggregation and inhibition. Other POCT devices measure 2. Lee-Lewandrowski E, Corboy D, Lewandrowski K, Sinclair J, McDermot S, Benzer TI.
platelet responsiveness to antiplatelet medications, such as aspirin and clopidogrel, or Implementation of a point-of-care satellite laboratory in the emergency department of an
are able to detect inherited and acquired platelet dysfunction, such as von Willebrands academic medical center. Impact on test turnaround time and patient emergency depart-
ment length of stay. Arch Pathol Lab Med. 2003;127(4):456-60
disease. 3. Kendall J, Reeves B, Clancy M. Point of care testing: randomized controlled trial of
clinical outcome. BMJ 1998;316:1052-7
Quality issues with POCT 4. NICE-SUGAR Study Investigators. Hypoglycemia and risk of death in critically ill
patients. N Engl J Med. 2012;367(12):1108-18
5. Shearer A, Boehmer M, Closs M, Dela Rosa R, Hamilton J, Horton K, McGrath R,
Schulman C. Comparison of glucose point-of-care values with laboratory values in criti-
cally ill patients. Am J Crit Care 2009;18(3):22430
6. Ng VL, Kraemer R, Hogan C, Eckman D, Siobal M. The rise and fall of i-STAT point-of-
care blood gas testing in an acute care hospital. Am J Clin Pathol 2000;114(1):128-38
7. Frankel HL, Rozycki GS, Ochsner MG, McCabe JE, Harviel JD, Jeng JC, Champion
HR. Minimizing admission laboratory testing in trauma patients: use of a microanalyzer. J
Trauma 1994;37(5):728-36
8. Rossi AF, Khan DM, Hannan R, Bolivar J, Zaidenweber M, Burke R. Goal-directed
medical therapy and point-of-care testing improve outcomes after congenital heart sur-
gery. Intensive Care Med 2005;31(1):98-104
9. Shore-Lesserson L, Manspeizer HE, DePerio M, Francis S, Vela-Cantos F, Ergin MA.
Thromboelastography-guided transfusion algorithm reduces transfusions in complex car-
diac surgery. Anesth Analg. 1999;88(2):312-9
10. Ak K, Isbir CS, Tetik S, Atalan N, Tekeli A, Aljodi M, Civelek A, Arsan S. Thromboelas-
tography-based transfusion algorithm reduces blood product use after elective CABG: a
prospective randomized study. J Card Surg 2009;24(4):404-10
11. Rhee AJ and Kahn RA. Laboratory point-of-care monitoring in the operating room.
Curr Opin in Anaesthesiol 2010;23(6):7418

Figure 10.2 Thromboelastography (TEG)

10.1 Point of care testing:
A. Reduces therapeutic turn around time
B. Has been consistently show to improve patient outcomes
C. Involves a multi-step process in which tests are ordered, samples drawn, labeled, and
transported to the lab.
D. Is always subject to a set of formal protocols, training, and documentation.

10.2. Advantages of POCT include all of the following EXCEPT:

A. Reduction in therapeutic turn around time
B. Use of smaller blood volumes minimizing of iatrogenic blood loss
C. No need for critical values notication system
D. Cost savings

10.3. Regarding POCT of coagulation studies, all of the following are true EXCEPT:
A. Activated clotting time (ACT) is often used in the operating room when monitoring the
effect of heparin therapy.
B. Thromboelastography (TEG) is a POCT that evaluates multiple levels of the coagula-
tion cascade and has been shown to accurately predict peri-operative and post-operative
bleeding in certain patient populations.
C. There are many POCTs available that test platelet function.
D. Traditional tests of coagulation (INR, PTT, platelet count, brinogen) allow complete
evaluation of the clotting cascade.

Section 3: Neuro Critical Care


Neurocritical Care

Management of Increased ICP

11. Neurocritical Care
Peggy White MD

Key Points You are called to evaluate a patient for emergent c-section. The parturient
is a 29 year old G2P1 who has a history of myasthenia gravis, status
Elevated ICP is managed by manipulation
post thymectomy 10 years ago and has since received plasmapheresis
on two separate occasions for exacerbation of her disease. She takes
of CSF, blood, interstitial fluid, bony skull or pyridostigmine and prenatal vitamins. She had clear liquids 6 hours ago,
neuronal cellular activity. otherwise her last meal was more than 8 hours ago.
Mortality and morbidity in SAH patients
is increased significantly by re-bleeding,
vasospasm and hyponatremia.

Ischemic stroke treated by tPA or mechanical

thrombectomy should have blood pressure
control below 180/110. Cytotoxic edema
occurs from 2-5 days post ischemia and can
cause significant brain swelling and possibly
Neuroanatomy and physiology
Patients with myasthenia gravis can safely The central nervous system is made of the brain, spinal cord, cerebral spinal uid (CSF) and supporting cells.
receive a depolarizing muscle relaxant. The adult human brain weighs approximately 1350 grams and receives between 12-18% of the total cardiac
output. In an average sized adult with a cardiac output of 5 liters per minute, this is about 750 ml of blood
per minute circulating through the four main cerebral arteries to the cranial vault. (Figure 11.1) Global ow
is 50ml/100 grams/min, ischemia occurs at 20 ml/100 grams/minute. If the delivery falls below this, the cells
will shift to anaerobic metabolism and pyruvate production will lead to acidosis and cell death. The brain
oxygen utilization 3.5 ml/100 grams/min.1

Neurons, supporting glia cells, blood vessels and CSF are compartmentalized inside the protective skull.
CSF is produced by the choroid plexus, mostly found in the lateral ventricles, the uid ows from the lateral
ventricles through the two foramens of Monroe into the third ventricle, through the cerebral aqueduct into the
fourth ventricle, and nally through the foramen of Magendie and two foramens of Luschka. CSF is absorbed
via the arachnoid granulations found on the inner surface of the dura. In the adult, the total CSF volume at any
given time is 150 ml, with an average production of 450 750 ml of CSF per day.1,2

Cerebral autoregulation is maintained by several factors and comprehensive discussion is too detailed for this
review. However, three pertinent factors are: pCO2, pO2, and mean arterial pressure. Cerebral vasoconstriction
(and thus a decrease in intracranial pressure, ICP) occurs with lowering of pCO2 levels. A decrease in pCO2
below 25 mmHg causes intense cerebral vasoconstriction resulting in ischemia. However in times of impend-
ing herniation, a moderate lowering of pCO2 to 30 mmHg can be life saving until other vasodilatation occurs. A MAP above 150 mmHg will result in cerebral vasoconstriction.
ICP reducing measures are taken.
The main effect of arterial oxygenation is noted at pO2 levels below 60 mmHg. At this
level there is intense vasoconstriction that may lead to cerebral ischemia. Levels above Increased ICP
60 mmHg cause little effect on cerebral vaso-responsiveness.
The Monroe-Kellie hypothesis describes the relationship between three substances:
Cerebral perfusion pressure is calculated by mean arterial pressure (MAP) minus ICP. blood, CSF and brain tissue, all contained in a bony box (the skull). Any increase in
The cerebral vasculature will constrict and relax to maintain perfusion at MAPs between one of the components will increase the intracranial pressure and compromise the other
50 70 and 150 mmHg. If the MAP decreases below 50 70 mmHg, intense cerebral two components. Lowering of ICP can be controlled by manipulation of the bony skull,
neuronal cellular activity, or uid volume (interstitial, CSF or blood).
Cerebral blood volume can be decreased by decreasing neuronal cellular activity or
cerebral metabolic rate of oxygen (CMRO2). CMRO2 can be slowed through the use of
hypothermia, barbituates, propofol and avoiding circumstances that may increase cel-
lular activity such as hyperthermia and seizures. A reduction in CMRO2 by 6 7% can
be achieved for each degree Celsius of temperature reduction. Hypothermia can cause
complete burst suppression at 18 20 C.1 The cerebral blood compartment can also
be decreased by facilitation of venous drainage, which is accomplished by elevation of
head of bed, avoiding internal jugular cannulation, avoiding extreme exion of the neck
and any constricting devices around the neck. In extreme circumstances muscle relax-
ation can be used to decrease muscular resistance to venous outow.
The brain tissue compartment can by decreased by hypertonic saline or osmotic diure-
sis, which decreases intracellular uid volume.
The CSF compartment can be decreased via neurosurgical intervention with CSF diver-
sion via an extra ventricular drain (EVD). As a last resort a craniectomy, or removal of
skull ap, can be performed to allow for controlled herniation out of the cranial vault.

Subarachnoid Hemorrhage
In the U.S. the incidence of subarachnoid hemorrhage (SAH) is estimated at 10 per
100,000.4 The true incidence is difcult to determine, since a quarter of patients die
prior to or en route to the hospital. Half of the patients who make it to the hospital will
be left with signicant disabilities.3

The hallmark sign of an acute SAH is the thunderclap, worst headache of their life with
photophobia 80% of the time. Other symptoms include: nausea, vomiting, meningis-
mus, brief loss of consciousness and focal neurological decits.3

Initial work up consists of a non-contrast CT scan. Once subarachnoid blood is identi-

ed on CT scan, a CT angiogram or IR angiography should be completed to identify
the location, size, and type of aneurysm to aid in operative planning (open craniotomy
versus endovascular). The aneurysm needs to be secured as soon as possible, usually in
the rst 24 to 48 hours. (Table 11.1 and 11.2)

Grading scales are used to estimate the risk for vasospasm and predicted morbidity. The
Fisher score predicts risk of vasospasm, and Hunt-Hess grade predicts patient mortality
and morbidity.

Mortality increases to approximately 80-90% if the aneurysm re-bleeds. Strict blood

Figure11.1 Circle of Willis pressure control is pivotal.3 The SAH guidelines do not state an absolute blood pressure
goal but, at our institution, a systolic pressure below 140 mmHg is maintained until the
aneurysm can be secured. Many agents can be used to reach this blood pressure goal. Intracerebral hemorrhage
Nicardipine infusion is preferred for its quick onset and offset, with minimal effect on Hemorrhagic stroke is the second most common form of stroke. It is difcult to dif-
heart rate. However, labetalol or nitroprusside could also be used. Keep in mind that ferentiate between hemorrhagic and ischemic stroke based on physical exam. The
nitrates can cause reex tachycardia and headache, which may complicate care. The use diagnosis must be conrmed by non-contrasted CT (the gold standard). Increased
of an antibrinolytic for clot stabilization can also be used for 24 hours while awaiting risk for hematoma expansion is highest during the rst three hours of symptom onset.
denitive intervention. Therefore, care is focused around early diagnosis and management to prevent expan-
sion of hematoma and subsequent decline in neurological status. Management during
The decision to clip (surgery) or coil (endovascular) the aneurysm is based on several these crucial hours includes; reversal of any anticoagulation, maintenance of ventilation,
oxygenation, hemodynamic support and avoidance of hypertension. The AHA stroke
Table 11.1 Hunt-Hess Grade guidelines state systolic blood pressure below 140 mmHg, but there is no conclusive
evidence to support a specic goal.5
Grade Clinical Findings
1 Asymptomatic or mild headache +/- nuchal rigidity There remains some controversy on medical versus surgical management. Surgical
intervention is recommended for posterior fossa hematomas, which compromise brain-
2 CN palsy, moderate to severe headache, nuchal rigidity
stem function and for large peripheral hematomas. Surgical management is often left to
3 Mild focal decit, lethargy or confusion the discretion of the neurosurgeon and depends on patient age, neurological decit, size
4 Stupor, moderate to severe hemiparesis, early decerebrate rigidity
and location of the hematoma.
5 Deep coma, decerebrate rigidity Once the patient is stabilized, management should focus on prevention of secondary
Add 1 grade for serious systemic disease or severe vasospasm
Adapted from Rosen, et al4 Table 11.2 Fisher Grade
Grade CT Findings
patient factors. Aneurysm location, neck size and aneurysm characteristics (saccular, 1 No subarachnoid blood
fusiform or blister) will help guide these decisions. 2 Diffuse or vertical layers < 1mm
3 Localized clot and/or vertical layer 1mm
Complications from SAH
Hydrocephalus: CSF diversion via extraventricular drain (EVD) or by serial lumbar 4 Intracerebral extension or intraventricular clot
punctures can improve the neurologic exam and relieve the hydrocephalus. The mecha- Adapted from Rosen, et al4
nism of hydrocephalus can be secondary to obstruction from mass effect occluding the
ventricle, a thick clot obstructing the ventricle or from dysfunctional CSF reabsorption injury such as: maintenance of euglycemia, avoidance of hyperthermia, continued cor-
via arachnoid granulations. rection of any coagulopathies, and CSF diversion for hydrocephalus. Patients are admit-
ted to the ICU for frequent neurological exams. For patients with Glascow coma scale
Vasospasm: The theorized mechanism is irritation to the arteries caused by blood (GCS) at or below 8, AHA guidelines recommend ICP monitoring and maintenance of
products or inammatory mediators in the subarachnoid space. It can occur in any of CPP above 50 70 mmHg.5
the cerebral arteries. The peak incidence of vasospasm is post bleed day 3 10, but
patients remain at risk up to 21 days. Typically patients are monitored for vasospasm Ischemic Stroke
and cerebral ischemia with hourly neurological examination, transcranial Doppler and Ischemic stroke is the most common form of stroke and the incidence is increasing
if indicated, CT angiography. Oral nimodipine 60 mg every 4 hours has been shown to as our population ages. The development of the AHA ischemic stroke guidelines has
reduce the incidence and long-term morbidity from vasospasm. Other measures shown increased awareness and improved patient survival.
to reduce morbidity include: statins, 5-7 days of antiepileptic medications, maintenance
of euvolemia (avoidance of hypovolemia).3
Any patient with a focal neurological decit suspicious of ischemic stroke should have
an immediate non-contrasted CT of the head to rule out a bleed and identify tissue at
Hyponatremia: from cerebral salt wasting (CSW), or SIADH. SIADH is euvolemic risk with perfusion weighted imaging. If the stroke onset has been within the last 3
hyponatremia and CSW is hypovolemic hyponatremia. For both diagnoses the goals of hours (4.5 hours with some exceptions), and there is no mass lesion or ICH, the patient
treatment are the same: to maintain euvolemia and normonatremia via hypertonic saline may qualify for systemic intravenous tissue plasminogen activator, tPA. The decision
or a mineralocorticoid. to administer tPA is largely governed by the time from onset of symptoms, NIH stroke
scale and other coexisting diseases. Common absolute contraindications to receiving
tPA include: persistent hypertension above 185/110, INR above 1.7 or receiving antico-

agulants recent stroke in past month, surgical procedures, and seizures.6 airway should be secured.

After tPA infusion, there is a 24 hour window where no anticoagulation (including Simultaneous seizure abortive therapy should also be immediately given. First line
DVT prophylaxis) or antiplatelet therapy is given. After this period, all patients should therapy is lorazepam, which has the most attractive pharmacokinetic prole. However,
receive aspirin. Some patients may benet from GpIIb/IIIa inhibitor therapy, but this midazolam and less favorably valium could be used depending on the clinical situation.
should be decided on a case by case basis.6 Early aggressive seizure abortive therapy is imperative, because the longer the seizure
continues, the higher the likelihood for development of status epilepticus.
Medical management of ischemic stroke includes continuous hemodynamic and
telemetry monitoring, supplemental oxygen to keep SpO2 above 94% (with intuba- If an identiable correctable cause of the seizure can be identied, such as hypogly-
tion if necessary), and maintenance of euglycemia (goal of 140-180 mg/dL). There is cemia or drug toxicity, the patient does not need maintenance antiepileptic therapy.
no conclusive evidence for blood pressure management. However, the AHA guidelines Otherwise, the patient should be started on maintenance antiepileptic therapy most ap-
recommend lowering blood pressure by 15% in the rst 24 hours, if the patient did not propriate for the type of seizure.
receive brinolysis and the blood pressure is above 220/120. If tPA has been given, the
blood pressure should be controlled below 180/110.6 Guillian-Barre
Guillian-Barre (GBS) is an acute immune mediated polyradiculoneuropathy that usually
Complications of ischemic stroke include hemorrhagic conversion and cerebral edema. presents 2 4 weeks after upper respiratory or gastrointestinal infections. Classical pre-
Typically these complications occur with large strokes, such as proximal middle sentation is ascending sensory and motor decits. Respiratory, bulbar and cranial nerve
cerebral artery (MCA) occlusion. Edema usually occurs between post ischemic day function can be impaired requiring intubation and mechanical ventilation. Autonomic
2 5. During this time, it is crucial to monitor neurological status and serum sodium. instability may complicate care and usually occurs at weeks 2 4 at peak weakness.
Hypertonic saline can be used to push serum sodium to 145 150 mEq/L in an attempt Symptomatology centers around the pathophysiology of myelin destruction by macro-
to reduce edema. Measures to prevent secondary injury as discussed above should be phages and lymphocytes.8
Diagnosis is made by nerve conduction studies and lumbar puncture. Lumbar puncture
Status epilepticus shows increased protein with normal glucose and minimal white blood cells. Prompt
According to the neurocritical care guidelines, status epilepticus is dened as a seizure diagnosis is essential, because therapeutic intervention should be started as soon as pos-
lasting longer than 5 minutes clinically or on EEG, or recurrent seizure activity without sible. Treatment includes plasmapheresis or IVIG as well as supportive care. There is no
recovery to baseline between seizures. The incidence of status epilepticus in the general benet in combining plasma exchange with IVIG.8
ICU population is around 10%, in the neuro ICU the incidence is around 12 25%.
Status epilepticus can be classied as: convulsive, non-convulsive or refractory status Acute respiratory failure secondary to muscle weakness can occur rapidly. Depolarizing
epilepticus. muscle relaxants are contraindicated because of the risk of hyperkalemia. Nondepo-
larizers can be used, but should be done with great caution as their use may result in
Convulsive status epilepticus presents with rhythmic tonic-clonic movements, mental prolonged weakness.1
status change, or focal neurological decits in the post ictal period.7
Myasthenia Gravis
Non-convulsive status epilepticus (NCSE) is categorized as seizures on EEG without Myasthenia gravis is an autoimmune disorder where autoantibodies are formed against
clinical features. They can be described as the wandering confused or the acutely ill the acetylcholine receptor on the post-synaptic neuromuscular junction. This results in
with severely impaired mental status. The latter of which is seen in critically ill patients generalized and/or bulbar weakness and fatigue, but not autonomic instability. There is a
who are sedated and intubated for other reasons. NCSE can further be divided into strong association of MG with thymus hyperplasia or thymomas.
positive (agitation, delirium, perseveration) and negative symptoms (aphasia, catatonia,
coma, confusion).
The clinical history and exam provide the rst clue to the diagnosis. Three studies can
be used for the diagnosis, anti-AChR antibody titers, the Tensilon test, and electromy-
Patients who dont respond to standard treatment (consisting of a benzodiazepine and ography. The tensilon test involves administration of a short acting acetylcholinesterase
one antiepileptic durg) are considered non-responders to standard treatment and are inhibitor (edrophonium) and then following for any improvement in symptoms. MG
considered to be in refractory status epilepticus (RSE).7 patients can safely receive depolarizing muscle relaxants, but will likely require a larger
dose. Caution should be used when administering nondepolarizers, as MG patients are
Initial treatment for seizures should be focused on maintenance of oxygenation, ventila- at risk for prolonged profound weakness.1
tion and hemodynamics. Initial management does not always necessitate intubation
and it may actually complicate the neurological exam after the seizures have been A paraneoplastic form of MG, called Eaton Lambert, results in weakness, but the patho-
controlled. However, if the patients oxygenation and ventilation is compromised the

genesis is autoantibodies formed against the presynaptic calcium channel.
Acute management of MG begins with the institution of IVIG, acetylcholinesterase
inhibitors and steroids. These patients often become too weak to manage their secretions 11.1 For the patient in the case presentation, which of the following options would be the BEST
and hypoventilate. Once the decision is made to secure the airway, the use of a seda- choice for GETA?
tive often is enough to create optimal intubation conditions. If a neuromuscular blocker
(NMB) is required, succinylcholine is the agent of choice, as non-depolarizering NMB A. There is no indication for neuromuscular relaxation in myasthenia gravis patients.
B. RSI with Succinylcholine and propofol.
can cause prolonged weakness.1 C. RSI with rocuronium and propofol.
D. She will need an awake beroptic intubation.
1. Miller RD, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Young WL. Eds: Millers Anes- 11.2 A 57 year old woman with a SAH is post bleed day 5, and post embolization day 4. Tran-
thesia, 7th edition. Churchill Livingstone: An Imprint of Elsevier, 2009. scranial dopplers show elevated velocity with a high lindegaard ratio consistent with vasospasm.
2. Greenberg, MS: Handbook of Neurosurgery. New York, Thieme Medical Publishers, Her serum sodium has decreased from 140 to 131 mEq/L in the last 36 hours. Her CVP is 6 cm
2010. H2O and she is one liter negative for her hospital stay. Urine Na is 60 mEq/L and urine osm
3. Connolly, ES, Rabinstein, AA, Carhuapoma, JR, et. Al: Guidelines for the management >100 mOsm/Kg. What is the next best intervention?
of Aneurysmal Subarachnoid Hemorrhage: A guideline for healthcare professionals from
the American Heart Association/American Stroke Association. Stroke 2012; 43: 1711- A. 3% saline bolus
1737. B. 23.4% saline bolus
4. Rosen, DS, Macdonald, RL. Subarachnoid hemorrhage grading scales: a systematic C. Fludrocortisone
review. Neurocritical Care 2005; 110118. D. Furosemide
5. Morgenstern, LB, Hemphill, C, Anderson, C et. Al: Guidelines for the management of
spontaneous intracerebral hemorrhage: a guideline for healthcare professionals From the 11.3.You are called to the bedside of a TBI patient with elevated ICP of 30 mmHg for the past
American Heart Association/American Stroke Association. Stroke 2010; 41: 2108-2129. 10 minutes. Which of the following is the next BEST thing to do?
6. Jauch, EC, Saver, JL, Adams, HP, et al: Guidelines for the early management of pa- A. Furosemide
tients With acute ischemic stroke: a guideline for healthcare professionals from the Ameri- B. Mannitol bolus
can Heart Association/American Stroke Association. Stroke 2013; 44: 870-947. C. 23.4% Saline
7. Brophy, GM, Bell, R, Claassen, J, et al: Guidelines for the evaluation and manage- D. Elevate the head of bed
ment of status epilepticus. Neurocrit Care 2012.
8. Dimachkie, MM, Barohn, RJ: Guillain-Barre syndrome. Current treatment options in
neurology 2013; 15: 338-349.
9. Barash PG, Cullen BF, Stoelting RK: Clinical Anesthesia, 3rd edition. Philadelphia,
Lippincott-Raven Publishers, 1997, pp 23-4

12. Management of Increased ICP
Matthew R Hallman MD

Key Points A 24 year-old man presents to the hospital following a motorcycle crash.
He was not wearing a helmet. His vital signs are HR 120 bpm, BP 88/50
Initial evaluation and management of an
mmHg, RR 24/min, SpO2 96% on ambient air, and T 37.1C. On exam, he
is noted to have obvious facial trauma and scalp abrasions, breath sounds
individual suspected of having an elevated bilaterally, normal heart sounds, weak pulses, GCS of 7 (E1 V2 M4) and
intracranial pressure (ICP) is targeted at both pupils are 5mm and reactive to light.
prompt identification and correction of
abnormalities in airway, breathing and
circulation (ABCs).

Recognizing an elevated ICP relies on

physical examination (Glasgow Coma Score),
neuro-imaging (CT/MRI of the head), and
invasive pressure monitors (predominantly
intraventricular drains, intraparenchymal and
subdural microtransducers).

Treatment of an elevated ICP is directed at Physiology

maintaining a favorable balance between Normal adult intracranial pressure (ICP) is 8-12 mmHg.1 The rigid cranium contains stable amounts of brain
cerebral oxygen supply and demand. This parenchyma, blood and cerebral spinal uid (CSF) that exist in equilibrium. An increase of any of the normal
involves maintaining cerebral blood flow by physiologic components or the addition of a pathologic component without simultaneously reducing the vol-
ume of another component results in an elevated ICP. This concept is known as the Monroe-Kellie Doctrine.
ensuring adequate cardiac output, reducing
cerebral vascular resistance through removal
Parenchymal volume is controlled primarily through regulation of vascular permeability and osmotic gra-
of intracranial components (blood, cerebral dients across the blood brain barrier (BBB). Cerebral edema results when the BBB is disrupted or over-
spinal fluid, intracellular/extracellular water), whelmed, and water accumulates within brain parenchyma. Cerebral edema is categorized as either cytotoxic
and reducing cerebral oxygen demands or vasogenic. Cytotoxic edema occurs from direct neural injury and cell lysis when osmoles enter and accu-
through control of fever, seizure, pain and mulate in the intracellular compartment. This may occur following traumatic brain injury (TBI) or ischemic
agitation. stroke. As water follows the osmotic gradient, swelling results. Similarly, if serum osmolality falls rapidly,
the BBB may be overwhelmed resulting in net movement of water from the intravascular to extravascular
space. Vasogenic edema results when hydrostatic forces favor water ow from the intravascular to the extra-
vascular space as may happen with increased intravascular pressure following a venous outow obstruction,
or when inammation causes increased vascular permeability such as occurs in perineoplastic territories.

Normally, CSF production (approximately 20 ml/hour by the choroid plexus in the ventricles) is in equilib-
rium with CSF absorption (approximately 20 ml/hour by the arachnoid villi in the subarachnoid cisterns).(1,2)
When production surpasses absorption, hydrocephalus results. Communicating hydrocephalus results from
the malfunction of the arachnoid villi, whereas obstructive hydrocephalus results from for invasive ICP monitoring.
the interruption of CSF ow from the choroid plexus to the arachnoid villi. Blood in the
subarachnoid space may cause communicating hydrocephalus, while mass lesions and The three most commonly used methods for invasive ICP monitoring are the external-
intraventricular blood often cause obstructive hydrocephalus. Transependymal ow of ized ventricular drain (EVD), intraparenchymal microtransducer, and subdural micro-
CSF from the ventricles to the parenchyma occurs with elevated intraventricular pres- transducer. An EVD allows for therapeutic drainage of CSF and in vivo calibration.
sure. This may also cause cerebral edema. However, there is a risk of infection and hemorrhage, and placement may be difcult in
patients with small ventricles. Intraparenchymal microtransducers, do not allow in vivo
Cerebral blood ow (CBF) and cerebral blood volume (CBV) are dynamic and occur on calibration, but appear to be more accurate than subdural microtransducers. They carry
a minute-to-minute basis. Four major mechanisms regulate CBF: 1) ow-metabolism a small risk of bleeding and infection. Device choice depends largely on the suspected
coupling; 2) pressure autoregulation; 3) CO2 reactivity; and 4) O2 reactivity.1,2 Flow- etiology of the ICP elevation as well as imaging ndings (e.g. in subarachnoid hemor-
metabolism coupling allows increased cerebral metabolic demands, as occurs with rhage and cases of hydrocephalus the ability to drain CSF is important and EVDs are
fever and seizures, to be met with cerebral vascular dilation and increased CBF and typically placed). In TBI, the ventricles may be displaced or compressed causing a
CBV. Conversely, resting states see less CBF and CBV. Pressure autoregulation allows difcult EVD placement. Therefore, an intraparenchymal or subdural microtransducer
constant CBF over a wide range of systemic mean arterial pressures (MAP). Higher is often used. If there is an elevated bleeding risk, the subdural microtransducer is often
MAP cause cerebral vasoconstriction whereas lower MAP cause cerebral vasodilation. selected as it carries the smallest risk of hemorrhage. Placing the monitor in an area of
This occurs over the MAP range of 65 150 mmHg in most people. The net effect is the brain that accurately reects the conditions in the brain, as a whole, is a challenge
relatively constant CBF over the entire range of pressures, but variable CBV (lower with all devices. The falx cerebri and tentorium cerebellum are physical barriers in
CBV at higher MAP and vice versa). When pressure autoregulation is disrupted, higher pressure transmission across varying areas of the brain. Monitoring on one side may
MAP result in increased CBV. Cerebral vascular CO2 reactivity causes vasodilation or not detect pressure elevations on the other. Hematomas and tumors may similarly limit
vasoconstriction. An increase in PaCO2 leads to an increase in CBF and CBV while pressure transduction necessitating careful evaluation of the quality of data returned
the converse occurs in a low PaCO2. This occurs over a PaCO2 range of 2570 mmHg. from the monitors.
However, this is a short-lived effect and CBF will return to baseline over the next 6-8
hours despite the PaCO2. Oxygen reactivity is similar, but vasodilation does not start
until PaO2 falls below 60 mmHg. Below this level both CBF and CBV rise sharply. Table 12.1. Indications for Invasive ICP Monitoring
When any of these control mechanisms fail it is possible for CBF to rise inappropriately
Traumatic Brain Injury: GCS < 9 after initial resuscitation AND an abnormal head CT
resulting in increased cerebral blood volume and an elevated ICP. OR a normal head CT AND two of the following: age > 40 years, SBP < 90 mmHg or
any motor posturing
Finally, ICP will rise when pathologic components such as hemorrhage and tumor Subarachnoid Hemorrhage
are present in the cranium. While small volume increases may be tolerated as CSF is
pushed into the extracranial thecal sac, the elastance ( P/ V) curve quickly steepens Symptomatic Hydrocephalus
resulting in large ICP rises with small subsequent volume increases. Massive Hemispheric Stroke
Acute Liver Failure
Optimal ICP and cerebral perfusion pressure (CPP) targets are not clear. Treatment is Imaging consistent with elevated ICP (cerebral edema, midline shift, compression of
generally indicated for ICP > 20 25 mmHg for 15 minutes or more. Maintenance of a cisterms)
CPP of 50 70 mmHg is recommended for most conditions.(1-3) However, ICP values
> 20 mmHg may be tolerated without problems in patients with normal CT-head imag- Management
ing, a fact that underscores the need to avoid simply treating numbers.(4) The same type Matching cerebral metabolic rate of oxygen consumption (CMRO2) to oxygen supply is
of physiologic rationale supports the avoidance of systemic hypotension, but specic the primary goal when ICP is elevated. Ensuring adequate cardiac output (CO) and he-
targets remain difcult to dene outside of the broad recommendations to maintain a moglobin (Hgb) is very important. While no specic CO targets exist, avoiding SBP <
sufcient MAP to keep a CPP of 50 - 70 mmHg at any given ICP. The utility of an ac- 90 mmHg is advised in most cases as deviation below this level is associated with worse
curate ICP assessment is therefore easy to understand. outcomes in TBI.3 Likewise, no specic Hgb target is supported by robust evidence, but
levels less than 7 g/dl, and possibly higher in some situations, should be avoided.
There are a number of theoretical methods for non-invasive ICP assessment, but CT
imaging is most commonly utilized. CT ndings suggestive of elevated ICP include Seizures, hyperthermia and agitation signicantly increase CMRO2, and should be
midline shift, hydrocephalus, cistern compression, edema, hemorrhage and other mass aggressively corrected.5 There is mixed evidence to support therapeutic hypothermia.
effects. Whenever imaging ndings or clinical exam raise suspicion for ICP elevation, Any potential benet to cooling a patient must be weighed against the potential for
invasive monitoring is the gold standard. Table 12.1 summarizes common indications other complications. Pain and agitation increase CMRO2 and also lead to ventilator
dysynchrony and increased ICP. As sedative and analgesic agents may obscure the
neurological exam, they should be titrated to the minimum effective dosage, but should

not be witheld.6 When sedation/analgesia alone is not effective in controlling ventilator risk. Figure 12.1 suggests a step-wise approach to the management of patients with an
dysynchrony it may be necessary to administer neuromuscular blockade (NMB).6 NMB elevated ICP.
should not be instituted without concomitant sedation as this can lead to signicant
anxiety and increased CMRO2 despite an outwardly calm patient.

Positioning the patients head above heart level is one of the least invasive ways to
acutely lower ICP.5 Similarly, ensuring good cerebral venous drainage by placing the
head in a midline position avoids vascular congestion that may contribute to an elevated
ICP.5 Recommendations to avoid placement of venous catheters in the internal jugular
vein over concerns of impeding venous outow are not evidence based. As most pa-
tients are mechanically ventilated it is important to consider that high levels of positive
end expiratory pressure (PEEP) and large tidal volumes may impede cerebral venous

The anti-inammatory effects of glucocorticoids are of theoretical benet in patients

with cerebral edema. In the setting of peri-tumor edema, they are in fact quite effec-
tive at reducing swelling and lowering ICP.6 However, they carry a risk of infection and
hyperglycemia and have been proven harmful in other settings such as TBI where they
should be avoided.3,6

Acute hyperventilation causes cerebral vasoconstriction, resulting in a decrease in CBV

and lower ICP. Conversely, hypoventilation and hypoxemia both lead to cerebral vaso-
dilatation and increased CBV. While hyperventilation lowers ICP for short periods, the
reduction in CBF may be harmful if maintained for too long. Further, the effect is lost
over 6-8 hours, and rebound acute respiratory acidosis with the associated cerebral va-
sodilatation and increased ICP may occur upon return to normoventilation. Hyperventi-
lation is, therefore, only recommended as a temporizing maneuver, but hypoventilation
and hypoxemia should be aggressively corrected.5
Figure 12.1 Stepwise Approach to Management of Increased ICP
Of the pharmacologic interventions, mannitol and hypertonic saline (HS) are most com-
monly used to acutely lower ICP.6 While they may also have rheological properties that
improve microcirculatory ow, their primary mechanism of action is the establishment
of an osmolar gradient favoring water egress from brain tissue. It is not clear which References:
solution is more effective. The choice of mannitol or HS is often guided by patient 1. Patel PY and Drummond J: Cerebral Physiology and the Effects of Anesthetic Drugs,
Millers Anesthesia, 7th edition. Edited by Miller RD. New York, Churchill Livingston
specic factors such as the starting serum sodium and intravascular volume status. Se- Publishers, 2010, pp 305-40
rum osmolality should be monitored with hyperosmolar therapy, as serum osmole loads 2. Patel PY and Drummond J: Neurosurgical Anesthesia, Millers Anesthesia, 7th edition.
greater than 320 330 mOsm may be harmful, and serum sodium should generally not Edited by Miller RD. New York, Churchill Livingston Publishers, 2010, pp 2045-88
be allowed to go above 160 mEq/L.6 3. Brain Trauma Foundation, American Association of Neurological Surgeons (AANS),
Congress of Neurological Surgeons (CNS), AANS/CNS Joint Section on Neurotrauma and
Critical Care: Guidelines for the Management of Severe Traumatic Brain Injury, 3rd edi-
When the above interventions fail to control ICP, more aggressive measures may be em- tion. J Neurotrauma 2007; 24(suppl 1)
4. Joffe AM, Hallman M, Glinas C, Herr DL, Puntillo K: Evaluation and treatment of
ployed. Electroencephalographic burst-suppression most commonly utilizes propofol pain in critically ill adults. Semin Respir Crit Care Med 2013; 34:189-200
or barbiturates to maximally decrease CMRO2.6 Both are associated with a signicant 5. Meyer MJ, Megyesi J, Meythaler J, Murie-Fernandez M, Aubut J, Foley N, et al: Acute
incidence of hypotension and neither have been shown to improve outcomes. Regard- management of acquired brain injury part I: an evidence-based review of non-pharmaco-
less of the agent chosen, continuous EEG monitoring is recommended in order to assess logical interventions. Brain injury 2010; 24(5): 694-705.
6. Meyer MJ, Megyesi J, Meythaler J, Murie-Fernandez M, Aubut J, Foley N, et al: Acute
burst-suppression and minimize sedative doses. management of acquired brain injury part II: an evidence-based review of pharmacological
interventions. Brain injury 2010; 24(5): 706-21
Surgical management may be necessary when ICP is refractory to all medical interven-
tions, when the initial presentation includes a pending herniation syndrome, or where
waiting for non-invasive measures to be effective is not considered reasonable.3,5 These
procedures are reserved for only the worst cases as they are not themselves without

12.1 Considering the patient in the case presentation at the start of this chapter, of the follow-
ing interventions, which is the MOST appropriate initial intervention?
A. Obtain CT imaging of the head
B. Place an ICP monitoring bolt
C. Initiate cooling measures
D. Administer a uid bolus

12.2 Of the following interventions, which is LEAST likely to increase ICP in a patient with a
traumatic brain injury?
A. Placing a central venous catheter in the internal jugular vein
B. Initiating a lung protective ventilator strategy (low tidal volume, high PEEP)
C. Placing the bed in Trendelenburg position for placement of a central line
D. Reducing a femoral fracture

12.3. In which of the following instances is administration of systemic glucocorticoids MOST

A. Subarachnoid hemorrhage with elevated ICP
B. Communicating hydrocephalus with elevated ICP
C. Traumatic brain injury with elevated ICP
D. Intracerebral tumor with elevated ICP

13. Delirium
Jace Perkerson MD and Ansgar Brambrink MD PhD

Key Points A 70 year old man with CAD, HTN, and NIDDM, is admitted to the ICU for
E. coli bacteremia and sepsis. He requires a norepinephrine infusion at 5
Delirium is commonly seen in ICU patients;
mcg/min to maintain MAPs > 60 mm Hg. On HD #2, ICU nurses note that
the patient is agitated. He pulls out his IV twice and tries to get out of bed
it is characterized by inattention, impaired without assistance. He has angry outbursts and claims the staff is trying to
cognition, and a fluctuating course. harm him. On exam he is lethargic. It takes several attempts to gain his
attention to answer questions. Once focused on a question he rambles and
Critically ill patients that develop delirium his speech is incoherent. There are no focal neurological decits.
have increased mortality rates, increased
hospital length of stay, cost of care, days
requiring mechanical ventilation, and
increased rates of long term cognitive

All ICU patients should be screened daily for

the presence of delirium.

Prevention of ICU delirium is achieved by Delirium is a very common problem among patients in the ICU. Due to its dramatic negative impact on
limiting modifiable risks, judicious use of all patient outcomes, it is important that all ICU providers be familiar with the clinical syndrome and its inher-
ent challenges. This article is intended to provide a brief overview about the clinical presentation and possible
deliriogenic medications, early mobilization, interventions for prevention and treatment of ICU delirium.
and promotion of a healthy sleeping
environment. What is delirium and why is it important?
Delirium is an acute clinical syndrome often seen in ICU patients. It is a form of organ dysfunction character-
ized by altered consciousness, impaired cognition, and a uctuating course. Three subtypes of delirium have
been described: hypoactive, hyperactive, and mixed. Hyperactive delirium is characterized by agitation, irri-
tability, perseveration and hypervigilance. Hypoactive is common among elderly patients, is easily missed by
ICU practitioners, and carries a poor prognosis when compared to the other subtypes. Hypoactive delirium is
notable for features such as slowed speech, lethargy, and diminished alertness. Elements of both, hyperactive
and hypoactive delirium characterize the mixed subtype.

Delirium is common in the ICU. The prevalence varies widely with different patient populations. For exam-
ple, nearly 80% of patients requiring mechanical ventilation are diagnosed with delirium while non-intubated
patients have an incidence closer to 20%. Overall prevalence ranges from 45% to 87%. Many adverse out-
comes have been associated with delirium in the ICU. These include increased risk of death during hospital-
ization, prolonged mechanical ventilation, increased rates of unplanned extubation, and increased healthcare
costs. In addition, patients diagnosed with delirium in the ICU often have increased rates of cognitive decits
and increased rates of death up to one year later.

What causes delirium?

The pathophysiology of delirium is not well understood. Multiple hypotheses exist for
mechanisms. Some research suggests decreased cholinergic activity in the develop-
ment of delirium. Other studies suggest alterations of the immune system may trigger
delirium based on observation of high levels of inammatory mediators (TNF-1) at the
onset of ICU delirium. Increased dopaminergic activity and an imbalance in serotonin
levels have also been implicated. Due to the complex nature of cognition it is likely that
the etiology of ICU delirium is multifactorial. Future research will likely allow better
understanding of the biological bases of the clinical syndrome.

Numerous factors have been identied that place an ICU patient at increased risk for the
development of delirium. Some factors are patient-related, such as age, medical history,
and conditions related to the acute illness, and can alert the clinician to a patient at
risk. Other factors may prove to be targets for prevention or treatment of delirium. For
example, the knowledge that daily interruption of pharmacological sedation in the ICU
is associated with decreased rates of delirium has led to change in how respective medi-
cations are used. Good examples are the current recommendations regarding the use
of benzodiazepines.1 Table 13.1 summarizes known risk factors, and Table 13.2 cites
medications that have been associated with ICU delirium. Considering this information
may aid the ICU provider in strategies to decrease the incidence of delirium in their

Table 13.1 Risk Factors for ICU Delirium

Patient Related Factors Acute Illness Factors Hospitalization /
Treatment Related
Alcohol/Tobacco Use Sepsis Impaired Sleep/Noisy
Increased Age Fever Medications (see Table 13.2)
Depression Shock Foley Catheters
Dementia Anemia Gastric Tubes
Respiratory Disease Immobility
Medical Disease Lack of hearing aids,
glasses, dentures
Electrolyte Abnormalities

How is delirium diagnosed? Figure 13.1 CAM-ICU Worksheet

Patients with delirium exhibit both, impaired cognition and abnormal behavior. These
abnormalities can be mild, moderate or severe, and their presence and course can vary
during the progression of the disease. Impaired cognition is often the rst sign. Patients sions, and hallucinations are also common features of delirium.
are noted to be disoriented to person, place, or time. Other signs are impaired memory
and reduced level of consciousness. Alteration in the sleep-wake cycle, paranoid delu- In current ICU practice, affected patients remain often unrecognized, particularly those
with the hypoactive subtype of delirium. A number of clinical tools have been devel-
oped to aid in diagnosis. While at least six different scales have been validated, cur-
rently the most commonly used instrument is the Confusion Assessment Method for avoid benzodiazepines likely will decrease the rate of delirium in the ICU setting.
the Intensive Care Unit (CAM-ICU) that was specically developed for use in nonver-
bal ICU patients. While initially complex appearing, the instrument is quite easy to use, A specic conundrum is the treatment of pain. While inadequate pain management has
and it takes only minutes to assess a patient. With > 90% sensitivity and specicity, this been shown to be a risk factor for ICU delirium, opioids, the most potent analgesics,
assessment tool is highly reliable for clinical use.2 CAM-ICU looks for the presence or have been closely associated with promoting ICU delirium. Equally well documented
absence of four key features of delirium: is that opioids, strictly used as analgesics, actually decrease the prevalence of delirium.
1. Acute or uctuating course Clinicians should therefore frequently assess ICU patients for pain and treat with potent
2. Inattention analgesics including opioids as needed. Accurately assessing pain and distinguishing it
3. Altered level of consciousness, and from ICU delirium is particularly challenging in the non-verbal patients as the 2 diag-
4. Disorganized thought. noses often present with similar symptoms, e.g. restlessness, agitation or anxiety. For
practical purposes, the available evidence suggest that opioids, when used for the treat-
ment of pain and not for the treatment of agitation or anxiety are safe and apparently do
Based on the results, a given patient is deemed either CAM-ICU positive (delirium not trigger delirium in ICU patients.
present) or CAM-ICU negative (no delirium). Figure 13.1 shows a typical CAM-ICU
assessment sheet (available in multiple languages).
Numerous non-pharmacologic strategies have been suggested to reduce the risk for
Routine use of a validated screening instrument such as the CAM-ICU will help the delirium in the ICU. Some examples are: early mobilization, physiologic sleep-wake
clinician to avoid undiagnosed and, therefore, untreated ICU delirium. rhythm and noise control.

How can delirium be prevented? Most patients in the ICU are conned to their beds, and while physical and occupational
Day-to-day clinical practice in the ICU should include considerations regarding deliri- therapy in the past were deemed unsafe for critically ill patients (especially those requir-
um prevention. Clinicians can aim to avoid medications, which are known to cause, or ing mechanical ventilation), early mobilization today is considered standard of care and
are associated with an increased rate of delirium. Nevertheless, immediate patient care identied as a means to reduce the incidence of delirium.1
needs may present obstacles to this goal. For example, the requirements for adequate se-
dation and pain relief need to be balanced against the risk for inducing delirium. While
sedatives and analgesics frequently cannot be avoided completely in the critically ill, ICU patients are exposed to an environment that does not promote healthy sleep pat-
the clinician can try reducing the dose or frequency as best as possible. Recent evidence terns unless this issue is specically considered by the treatment team. Numerous
suggests that daily stoppage of sedatives, when combined with a spontaneous breathing alarms, communication between personnel, illuminated rooms, hallways and moni-
trial, decreases the rate of ICU delirium.1 tors, as well as repeated oral medications will reduce the amount and quality of sleep.
Encouraging a quiet, calm environment that employs lighting strategies to simulate a
day-night cycle, thereby promoting adequate sleep, can further reduce delirium in ICU
Table 13.2 Medications Commonly Associated with ICU Delirium patients.
Prescription Over-The-Counter
In addition to reducing or eliminating deliriogenic medications and employing non-
benzodiazepines diphenhydramine pharmacologic methods, options for prophylactic medical treatment have been explored.
barbiturates mandrake Among the drugs tested, the anti-dopaminergic, antipsychotic haloperidol has been
narcotics henbane studied most intensely with mixed results. While some studies suggested a signicant
antiparkinson agents jimson weed effect in delirium prevention compared to placebo, others did not observe any benet
antihistamines belladonna extract resulting from preemptive haloperidol medication.2 Based on these results, prophylactic
H2 blockers valerian
scopolamine loperamide anti-delirium treatment using antipsychotic drugs are currently not recommended.
tricyclic antidepressants Once diagnosed, how is delirium treated?
digitalis First and foremost, the treatment of ICU delirium starts by addressing critical illness.
beta-blockers Signicant imbalances in volume status, electrolytes, glucose, nutrition status, and oxy-
muscle relaxants gen delivery should be optimized rst. Next, drugs that are known triggers of delirium
steroids should be discontinued or their dosages decreased if possible. Protecting the patient
from self-injury is another important aspect in the management of this syndrome. While
physical restraints may sometimes be indicated for safety, their use also has been linked
Similarly, clinicians can try avoiding specic drugs that alone, or in combination with to an increased incidence of delirium. Therefore restraint use should be viewed as a last
others, increase the risk for delirium. Strong evidence suggests that benzodiazepines resort, and other techniques for behavior management should be employed. Close obser-
(e.g. midazolam, lorazepam) can cause delirium. Therefore, sedation strategies that vation by a nurse, family member, or other healthcare provider (sitter) is often very

Medications are often used for the treatment of ICU delirium, although solid evidence
proving their effectiveness is lacking. Nevertheless, haloperidol is currently most 13.1 Of the following subtypes of ICU delirium, which carries the worst prognosis?
commonly used as the rst line therapy for the hyperactive form of delirium. In addi-
tion, newer antipsychotics (so called atypicals) have recently received great attention. A. Hyperactive
B. Hypoactive
While the data is still inconclusive, agents like risperidone, olanzapine, and quetiapine C. Mixed
are currently considered effective treatment alternatives. D. Organic

As a matter of principle, the potential benet of antipsychotics must always be balanced 13.2 Which of the pairings below are BOTH known to be risk factors for the development of ICU
against their inherent risk for QT prolongation, cardiac arrhythmia and other side effects
relevant to the critically ill patient. Due to the lack of tangible evidence, current practice A. Depression AND IV potassium
guidelines published by the Society of Critical Care Medicine make no specic recom- B. Mechanical ventilation AND early rehabilitation
mendation for the use of these agents for the treatment of ICU delirium. Rather, they C. Benzodiazepines AND foley catheters
recommend against the use of these agents in patients who are at risk for torsades de D. Steroids AND analgesic therapy for post-surgical pain

Benzodiazepines and cholinesterase inhibitors are counterproductive in the management 13.3. Of the following, which can help prevent the onset of delirium in the ICU?
of delirium for the reasons mentioned above, and should be avoided.
A. Avoidance of benzodiazepines
B. Adequate analgesia
C. Promotion of a normal sleep/wake cycle
D. Early mobilization and rehabilitation
References: E. All of the above
1. Brummel NE, Girard TD: Preventing Delirium in the Intensive Care Unit. CritCare
Clin. 2013; 29(1): 51-65.
2. Cavallazzi R, Saad M, Marik P: Delirium in the ICU: an overview. Ann Intensive Care.
2012; 2(1):49. 13.4 Of the following medications commonly used in the treatment of delirium, which agent
3. Barr J, Fraser GL, Puntillo K, et al: Clinical practice guidelines for the management of should be avoided in the hemodynamically unstable patient?
pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med.
2013; 41:263-306. A. Haloperidol
4. Banh, HL: Management of Delirium in Adult Critically ill Patients. J Pharmaceut Sci. B. Olanzapine
2012; 15(4) 499-509. C. Quetiapine
5. Website: ICU Delirium and Cognitive Impairment Study Group. http://www.icude- D. Risperidone E. Dexmedetomidine
6. Ely EW, Margolin R, Francis J, May L, Truman B, Dittus R, Speroff T, Gautam S,
Bernard GR, Inouye SK: Evaluation of delirium in critically ill patients: validation of the
Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med
2001; 29(7):13701379.

Section 4: Airway and Pulmonary


Airway Management

Tracheostomy Management

Management of Mechanical Ventilation

Weaning from Mechanical Ventilation

14. Airway Management
Elizabeth Hankinson MD and Aaron Joffe DO

Key Points A 22-year-old male is involved in a motor vehicle accident and arrives to
the hospital with a suspected C4 vertebral fracture. He is admitted to the
The 3 major indications for airway
ICU for neurologic evaluation and airway management. The patient is 87
kg and 182 cm with good mouth opening. He is currently in a cervical collar
management in the ICU are need to: (1) deliver and his Mallampati score is 2. An awake beroptic technique is selected and
a high FIO2; (2) positive pressure ventilation; his airway is topicalized with aerosolized and viscous lidocaine. An infusion
and/or (3) provide an artificial airway/ to secure of dexmedetomidine is started during the topicalization and he is placed on
an airway nasal cannula at 4L/min. He is sedated yet spontaneously ventilating while
a beroptic bronchoscope is passed through the mouth and the vocal cords.
There are various instruments and methods An 8.0 cuffed endotracheal tube is passed over the bronchoscope.
available to place an endotracheal tube.
Available equipment, patient factors, and
provider preference will ultimately dictate the
final course of action.

Always be familiar with a back-up plan

should the first plan be unsuccessful.
Institution of invasive mechanical ventilation can be a lifesaving procedure in critically ill patients. It should
Complications in the ICU are more common be noted, however, that the reported incidence of airway related morbidity and mortality is several fold higher
when performed emergently outside of the operating room. This is not surprising in that critically ill pa-
than in the operating room. tients frequently have limited physiologic reserve. Additionally, the primary indication for the procedure is
often hemodynamic instability, hypoxic or hypercapnic respiratory failure, or the need for an articial airway
consequent to airway edema, copious secretions, altered mental status, or injuries to the head and neck. Thus,
awakening the patient after induction or deferring the procedure until conditions are more optimal is not an

Indications for Invasive Airway Management

The indications for invasive airway management can be broadly categorized into three categories: the need
to deliver a high fraction of inspired oxygen (FiO2), the need for positive pressure ventilation, or need of an
articial airway/secure an airway (Table 14.1). These categories are not necessarily mutually exclusive. For
example, a patient suffering neuromuscular weakness due to Guillain-Barr syndrome may have atelectasis,
a decreased FRC, elevated intrapulmonary shunt fraction, and increased elastic work of breathing (need for
positive pressure). Additionally, bellows fatigue may result in alveolar hypoventilation (need for ventilation)
while cranial nerve involvement can severely impair the ability to control and coordinate the muscles of the
upper airway (need for an articial airway).
pharmacologic prole of the medications chosen, the side effects, and how to counter
Table 14.1: Indications for Airway Management
Need for high FiO2 Need for Ventilation Need for Articial Airway
- hypoxemic respiratory - hypercapneic respiratory - airway obstruction A variety of techniques may be used to secure the airway. However, orotracheal intuba-
failure failure - suppressed upper airway tion using some type of (modied) rapid sequence induction/intubation (RSI) is by far
- CHF - neuromuscular disease reexes the most common. Routine asleep intubation is performed when the provider feels
- pulmonary contusion - cervical spinal cord injury - facial or neck trauma condent that the airway can be secured after induction. Optimal patient position is the
- ALI/ARDS - diaphragmatic paralysis - oropharyngeal or laryngeal snifng position with the neck exed and the head extended at the atlanto-occipital
- Morbid obesity - COPD exacerbation edema joint to align the oral, pharyngeal and laryngeal axes.
- severe asthma - TBI, stroke, SAH
exacerbation - GCS < 9
- drug intoxication - sustained seizure activity
- copious secretions

Airway Examination
The external airway exam has poor positive and negative predictive value. For the pur-
poses of procedural planning, airway difculty should be expected. Nonetheless, a rapid
but thorough examination of the airway should be done whenever possible prior to air-
way management. Traditionally reported risk factors for difcult mask ventilation and
difcult intubation are presented in Table 14.2. More recently, a seven item score was
shown to be accurate and precise in identifying patients at risk for difcult intubation in
the ICU (Table 14.3). Mallampati grading is presented in Figure 14.1. Examination is
classically performed with the patient sitting upright, neck extended and tongue protrud-
ing without phonation. However, assessment of the patient in recumbent position, as
may be necessary in the critically ill, is at least as good.
Figure 14.1 Mallampati Grading
Table 14.2: Characteristics Predictive of Difculty Ventilating or Intubating
Predictors of Difcult Ventilation Predictors of Difcult Intubation
- BMI > 30 - facial trauma/swelling After induction, the ability to bag-mask-ventilate is veried. A neuromuscular blocking
- macroglossia - airway swelling or bleeding agent (NMBA) is then given with bag-mask-ventilation continued until the airway is
- edentulous - anatomical anomalies secured with the placement of the endotracheal tube. This step of test ventilating prior
- facial trauma/swelling - thyromental distance < 3FB to administration of the neuromuscular blocking drug is commonly omitted when rapid
- snoring - mouth opening < 2FB sequence induction/intubation techniques are used. Securing the airway can be facili-
- limited jaw protrusion - decreased neck ROM tated via direct or video laryngoscopy, intubating LMA, Eschmann stylet or a exible
- signicant overbite beroptic bronchoscope. Direct laryngoscopy is the most common initial method when
- short, thick neck
- Mallampati class III or IV
Table 14.3: MACOCHA Score for Predicting Difcult Intubation
BMI: body mass index; FB: ngerbreadths; ROM: range of motion
Factors Points
Patient Mallampati Score III or IV 5
Intubation in the ICU Obstructive Sleep Apnea 2
The rst step is to determine the urgency of the clinical situation. Whenever possible, an
Cervical Spine Immobility 1
evaluation of the airway should be performed and the patients vital signs, medications,
allergies, recent labs and mental status reviewed. The ICU staff and respiratory thera- Mouth Opening < 3cm 1
pist should be notied of an impending intubation. Following an intubation checklist
Disease Coma 1
(See example of one in Figure 14.2) will ensure a standardized approach to the setup
and communication surrounding the procedure. Such an intubation bundle has been Hypoxemia 1
shown to reduce severe hypoxemia and cardiovascular collapse in the ICU (Table 14.4) Practitioner Experience Non-Anesthesiologist 1
ICU patients may be obtunded and require little or no medication in order to induce
anesthesia for tracheal intubation. If medications are required, consider the patients he- Total scored from 0-12, with higher scores predicting increased difculty.
modynamic status, renal function and electrolytes. The intensivist should understand the Adapted from deJong, et al.9

Figure 14.2 Emergency Induction Checklist

the external airway examination is reassuring. Regardless, the immediate availability of an increased rate of complications. Every health-
adjunct airway equipment is of vital importance and should not be overlooked. care provider should be prepared with appropriate
anesthetic agents, vasopressors and difcult airway
When a grade 1 view is acquired, the tube can be directly inserted. This may not be equipment, have the most experienced personnel
the case with a grade 2 view and an Eschmann stylet may be employed. When a grade available, have appropriate staff present and have a
3 view is acquired, the Eschmann stylet is recommended, but may not be sufcient and backup plan prepared. When faced with a dif-
the operator may need to move to another technique altogether, whereas with a grade 4 cult airway, either anticipated or discovered after
induction, the managing physician should have
some familiarity with the difcult airway algorithm
Table 14.4: ICU Intubation Bundle Worksheet endorsed by the ASA (Figure 14.4).
PRIOR to intubation:
- two operators available Complications of Endotracheal Intu-
- small uid bolus (250-500ml) in the absence of cardiogenic pulmonary edema
- long-term sedation available bation
- pre-oxygenation with 100% oxygen for 3-5 minutes if time allows The incidence of complications associated with
endotracheal intubation is quite small when done
INTUBATION: electively in a controlled environment. However,
- RSI: propofol, etomidate or ketamine, followed immediately by succinylcholine (in
the absence of hyperkalemia, severe acidosis, neuromuscular disease, spinal cord there is a several fold increase when done emer-
trauma or burn injury over 48h, in which case rocuronium may be substituted) gently on critically ill patients outside the operating
- Cricoid pressure (Sellick maneuver) until conrmation of secure airway room. Complications associated with endotracheal
intubation can occur either during intubation or
AFTER intubation: after the endotracheal tube is in place (Table 14.5).
- conrmation with capnography* followed by CXR
- initiation of long-term sedation
- initiation of mechanical ventilation (initial Vt 6-8ml/kg)
Figure 14.3 Cormack-Lehane
*capnography may be inaccurate if cardiac output is extremely low or non-existent grading of vocal cord view
such as in cardiac arrest. RSI: rapid sequence induction; CXR: chest x-ray; Vt: tidal

view, an alternative technique should be immediately employed. (Figure 14.3) Blind

intubation techniques are discouraged, unless there is no other option.

Patients requiring emergent intubations are often not NPO and need a rapid intubation
process to protect against aspiration of gastric contents during induction referred to as
rapid sequence induction. Rapid sequence induction is done by administering the induc- Table 14.5: Complications of Endotracheal Intubation
tion agent, immediately followed by a rapid-acting neuromuscular blocking agent while During Intubation
applying cricoid pressure (Sellick maneuver) with no attempts at bag mask ventilation
prior to securing the airway. Trauma: dental, lip or oral mucosa, perforation or dislocation of pharyngeal, laryngeal
or tracheal structures

An awake intubation is reserved for patients with airway pathology resulting in sig- Pulmonary: hypoxia, esophageal intubation, laryngospasm, bronchospasm
nicantly increased risk of failed intubation and/or ventilation after induction. This Cardiovascular: hypotension, hypertension, arrhythmias
includes patients with signicant face and neck pathology, oropharyngeal obstruction,
Neurologic: increased ICP, passage of tube into cranial vault during nasal intubation
and those with severely limited mouth opening. The sensory nerves of the airway - glos- in patient with basilar skull fracture
sopharyngeal, superior laryngeal and the recurrent laryngeal can be anesthetized prior
to the procedure to prevent excessive gagging and coughing. An awake intubation is Post Intubation
performed in a variety of ways, including blind nasal, direct laryngoscopy, or most com- kinking or blockage of tube
monly, with a exible beroptic bronchoscope. This technique takes time and requires
a patient who is somewhat cooperative and stable. Sedation with minimal changes in misplacement/displacement of tube
respiratory drive or muscle tone can be achieved with low-dose infusions of either dex- ischemia of tracheal tissue
medetomidine or remifentanil.
vocal cord injury
Airway management outside of the OR (i.e., the ICU) is often more challenging and has sinusitis (nasal intubation)

1. Buckley TA, Short TG, Rowbottom YM, Oh TE: Critical incident reporting in the inten- Questions
sive care unit. Anaesthesia 1997; 52:403-409
2. Levitan R, Ochroch EA: Airway management and direct laryngoscopy. A review and 14.1 After administering intravenous medications for a rapid sequence induction, you attempt
update. Crit Care Clin 2000; 16(3):373-88 to intubate the patient via direct laryngoscopy. You have a grade 4 view and are unable to suc-
3. Mort, T: Continuous airway access for the difcult extubation: the efcacy of the air- cessfully intubate the trachea on your rst attempt. The patients saturation is now 84%. After
way exchange catheter. Anesth Analg 2007; 105:1357-62 calling for help, what is your next step in airway management?
4. Hassid VJ, Schinco MA, Tepas JJ, Griffen MM, Murphy TL, Frykberg ER, Kerwin AJ:. A. Placement of an LMA
Denitive establishment of airway control is critical for optimal outcome in lower cervical B. Attempt to intubate with a different blade (i.e. Macintosh to Miller)
spinal cord injury. J Trauma 2008; 65:1328-32 C. Fiberoptic intubation
5. Cormack RS, Lehane, J: Difcult tracheal intubation in obstetrics. Anaesthesia 1984: D. Attempt face mask ventilation
6. Kheterpal S, Han R, Tremper KK, Shanks A, Tait AR, OReilly M, Ludwig TA: Incidence
and predictors of difcult and impossible mask ventilation. Anesthesiology 2006;105:885- 14.2 Which of the following statements regarding cricoid pressure for rapid sequence intubation
91 is true?
7. Apfelbaum JL, Hagberg CA, Caplan RA, Blitt CD, Connis RT, Nickinovich DG, et A. Despite adequate cricoid pressure, aspiration may still occur, particularly in patients
al: Practice guidelines for management of the difcult airway: an updated report by the withfull stomachs or active vomiting.
American Society of Anesthesiologists Task Force on Management of the Difcult Airway. B. Cricoid pressure should be released immediately after the endotracheal tube is inserted.
Anesthesiology 2013; 118:251-70 C. When applied correctly, cricoid pressure will always prevent aspiration during intubation.
8. Walz JW, Zayaruzny M, Heard SO: Airway management in critical illness. Chest 2007; D. None of the above
9. De Jong A, Molinari N, Terzi N, Mongardon N, Arnal JM, Guitton C, et al: Early iden- 14.3 A man is admitted to the ICU following a motor vehicle collision with blunt trauma to the
tication of patients at risk for difcult intubation in the ICU: development and validation face, head, and neck. Although still protecting his airway, he does have a decreasing mental
of the MACOCHA score in a multicenter cohort study. Am J Respir Crit Care Med 2013; status. You decide to electively intubate this patient. Which of the following statements regard-
187:832-9 ing the management of this patients airway is true?
A. An awake blind nasal intubation is an acceptable method and route.
B. An asleep intubation via direct laryngoscopy with propofol and vecuronium is not unrea-
C. An awake beroptic intubation through the mouth is safe.
D. A rapid sequence induction is not indicated for an asleep intubation.

14.4 A 37 year-old woman presents to the ER 2 hours after sustaining a 3rd degree burn to
45% of her body in a house re. On exam, you observe soot in the airway and singed nasal
hairs. She is awake, alert, and oriented to person, place, and time. Her voice is clear and easy to
understand. Which of the following is most appropriate?
A. Clear the patient for discharge
B. Continue to monitor the patient in the ER
C. Electively intubate this patient
D. Electively administer ketamine

14.5 You are called to the ICU to intubate a patient with respiratory distress. The patient is a 27
year-old woman G1P0 at 30-weeks gestational age. She has a history of cystic brosis, chronic
hypertension, and newly diagnosed gestational diabetes. Her last meal was 10 hours ago. You
prepare your equipment for intubation. Which of the following is most accurate regarding your
airway management?
A. A standard induction using a slower-acting neuromuscular blocking agent is appropriate
since the patients last meal was over 8 hours ago.
B. Patients with diabetes always have delayed gastric emptying and therfore should re-
ceive a rapid sequence induction.
C. Pregnancy places this patient at risk for aspiration and a rapid sequence induction is
D. Pregnancy causes dilation of the airway and a larger endotracheal tube is recommend-

Figure 14.4 ASA Difcult Airway
Algorithm, 2013 7

15. Tracheostomy Management
Andrea Tsai MD, Mandeep Singh MD and John Turnbull MD

Key Points A 26 year-old man, intubated in the emergency department for a GCS
of 5 following a motor vehicle crash, is admitted to the intensive care
There are no major outcome differences
unit. Persistently elevated intracranial pressures requiring deep sedation
and paralysis, ventilator-associated pneumonia, and acute lung injury
between surgical versus percutaneous complicate his ICU course. On ICU day 9, he remains intubated due to
tracheostomies continued encephalopathy. An uncomplicated percutaneous bedside
tracheostomy is performed with placement of a size 6 cuffed, unfenestrated
No consistent evidence for major outcome Shiley tracheostomy tube. On post-procedure day 2, his tracheostomy tube
benefits to early (prior to 10 days) versus late is accidentally dislodged. His airway is re-secured via oral endotracheal
(after 10 days) tracheostomy intubation. His Shiley tracheostomy tube is then replaced under
bronchoscopic guidance.
A decannulated fresh (within 7 days of
tube insertion) tracheostomy is an airway
emergency and generally the first maneuver
should be securing the airway via oro-tracheal

A tracheostomy is the creation of an opening into the trachea such that the tracheal mucosa is continuous with
the external epithelium. It is an increasingly popular procedure that may be performed open (surgically) in the
operating room or percutaneously at the bedside. A tracheostomy decreases the work of breathing by decreas-
ing the volume of dead space and increases the ease of respiratory care (e.g., tracheal suctioning). However, it
results in the loss of some upper airway functions, such as ltration and humidication of inspired air. Trache-
ostomies are commonly seen in the ICU for patients requiring prolonged mechanical ventilation.

Clinical indications for tracheostomy include the following.1
Prolonged or expected prolonged intubation/mechanical ventilation
Upper airway obstruction
Inability to manage secretions (including aspiration or excessive broncho-pulmonary secretions)
Ventilator support to facilitate rehabilitation
Inability to be orally or nasally intubated
As an adjunct to manage head and neck surgery or signicant head and neck trauma
Chronic mechanical ventilation due to chronic respiratory failure period.5

The benet of early (within one week of endotracheal intubation) versus late trache- Open (surgical) tracheostomies typically involve transport of the patient to the operating
ostomy remains an issue for debate. Tracheostomy placement may improve patient room where pre-tracheal tissues are surgically dissected and the tracheostomy tube is
comfort while decreasing the use of sedatives, and facilitating weaning from mechani- inserted into the trachea under direct vision. Percutaneous tracheostomies can be done
cal ventilation. It may also reduce trauma to the upper airway, the incidence of noso- at the bedside and employ a Seldinger technique followed by blunt dilation over a wire
comial pneumonia, and ICU or hospital length of stay. A 2005 systematic review and to open pre-tracheal tissues for the passage of a tracheostomy tube. Wire cannulation
meta-analysis suggested that early tracheostomy reduced the duration of mechanical and tube placement are usually visualized in real-time with bronchoscopy. Research has
ventilation and hospital stay yet it failed to demonstrate an improvement in mortality yielded conicting results regarding the superiority of open or percutaneous tracheosto-
or the occurrence of nosocomial pneumonia.2 A 2012 Cochrane review drew similar mies, thus the choice of technique is typically based on institution and surgeon prefer-
conclusions, but noted that available data is limited and could lead to bias.3 To address ence. A recent meta-analysis suggests that percutaneous tracheostomies may have a
this question, a recent large randomized controlled trial (TracMan) comparing early ( lower occurrence for wound infection (OR 0.28, 95% condence interval 0.16 to 0.49, p
4 days) to late ( 10 days) tracheostomy was performed. Again, there was failure to < 0.0005) with otherwise equal incidence of bleeding, major peri-procedural and long-
demonstrate improvement in 30-day mortality, 2-year mortality or ICU length of stay.4 term complications.6
These studies also commented on the difculty in accurately predicting patients who
will require long-term endotracheal intubation. Tracheostomy Tube Types and Management
Contraindications5 Tracheostomy tubes vary based on material used for construction, length, diameter,
and presence or absence of an inner cannula, cuff and fenestrations.7 Components of a
Patient or surrogate refusal to consent
Infection at the site of potential tracheostomy placement
Anatomic aberrations obscuring neck anatomy,
Patient instability, including high oxygen requirements or ventilator settings

The tracheotomy is typically performed between the 2nd and 3rd or 3rd and 4th tracheal
ring interspace. (Figure 15.1) Placement too high increases the risk of subglottic steno-
sis. Placement too low increases the risk of damaging vascular structures (the brachioce-
phalic vein or innominate artery) and accidental decannulation in the early postoperative

Figure 15.2 Pieces of a Tracheostomy Tube

Figure 15.1 Anatomy of Tracheostomy Site

tracheostomy include the following (Figure 15.2): - Tube obstruction
Single cannula
Double cannula (inner and outer cannulas) Intraoperative complications include bleeding, injury to surrounding structures (the
Neck ange thyroid, esophagus, recurrent laryngeal nerves, and surrounding vasculature), pneumo-
Obturator thorax, and air embolism. Bleeding is the most common complication, typically the
result of injury to the anterior jugular veins or thyroid isthmus.5 Care is taken to remain
Cuff midline during tracheostomy and, where applicable, perform suture ligation of the
Pilot Balloon thyroid isthmus. Other structures at risk when straying off midline during tracheostomy
include the recurrent laryngeal nerves, carotid sheath and internal jugular vein. Injury to
Tubes with variable lengths proximal and distal to their bend accommodate varia- the internal jugular vein may result in the rare complication of air embolism. Injury to
tions in tracheal tissue depth and anatomy. A longer proximal portion or an adjustable the posterior tracheal wall may result in a trachea-esophageal stula.
ange will accommodate patients with thicker pre-tracheal tissues, while a longer distal
portion may facilitate ventilation in patients with tracheal anomalies. Tube diameter, Early postoperative infection as a complication of tracheostomy is rare; prophylactic
dened both by inner and outer cannula diameters, affects resistance to airow and antibiotics are not typically used during this procedure.5, 7, 8 Subcutaneous emphysema
work of breathing. Although an inner cannula decreases the effective diameter and thus can be a result of excessive positive pressure ventilation or false lumen passage. Mucus
increases resistance to airow, the removable cannula allows for convenient respiratory plugging leading to acute airway obstruction is a common occurrence with new trache-
care, as inspissated mucous can be removed with a simple inner cannula exchange or ostomies. Deep suctioning, warm humidied air/oxygen, or nebulized normal saline
cleaning. treatments may decrease this occurrence.
There are no major outcome differences between surgical versus percutaneous
tracheostomies Early tracheostomy tube displacement is an airway emergency as the tracheostomy tract
No consistent evidence for major outcome benets to early (prior to 10 days) is not yet epithelialized and blind recannulation may result in the creation of a false
versus late (after 10 days) tracheostomy lumen. The rst approach after accidental early decannulation should be oro-tracheal in-
A decannulated fresh (within 7 days of tube insertion) tracheostomy is an airway tubation. 7, 8 Experienced providers should only undertake the passage of a tube through
emergency and generally the rst maneuver should be securing the airway via oro- the tracheostomy site when tracheal rings may be visualized. Dislodged tracheostomies
tracheal intubation. older than 7 days can usually be blindly recannulated with a tracheostomy tube (facili-
tated by an obturator) or an endotracheal tube placed through the tracheostomy site.
Nearly all tubes in the ICU, especially newly placed ones, will have an inatable cuff
to facilitate positive pressure ventilation. As weaning from mechanical ventilation Late postoperative complications include the following:
occurs, the cuff may be deated or the tube exchanged for a cufess, fenestrated, and/
or smaller diameter tube; however, tubes should only be exchanged 7 days following - Granuloma formation with tracheal stenosis
initial cannulation to ensure epithelialization of the tracheostomy site. Tube fenestra-
tions increase the ease of airow around and through the tube. A smaller diameter tube - Tracheomalacia
may improve a patients ability to phonate with the use of a Passy-Muir valve, which is - Fistula formation with multiple adjacent structures.
a one-way valve attached to a tracheostomy that allows inhalation through the tracheos-
tomy but blocks airow during exhalation and thus forces air through the vocal cords. Granulomatous tissue formation leading to tracheal stenosis occurs due to the bodys
It is contraindicated to have a tracheostomy cuff inated with a 1-way valve in place, innate reaction to foreign bodies. Such ndings may be asymptomatic, but occasionally
as this renders the patient unable to exhale. Eventually, if the indications for initial tra- require intervention such as correcting the tube size, cautery of granulation tissue, and/
cheostomy have been reversed, decannulation of the tracheostomy can be considered. In or laser ablation.5 Tracheomalacia results from cuff over-ination or excessive traction
general, a mature stoma can close up to 50% within 12 hours and up to 90% within 24 by ventilator tubing with resultant tissue ischemia and necrosis. Fistula formation, a
hours; complete closure may take up to 2 weeks.8 rare late complication of tracheostomies, may form between the trachea and the esopha-
gus, skin, and innominate artery. Tracheo-esophageal stulas can present as tube feeds
Complications in the tracheostomy tube; other signs and symptoms include copious secretions, air leak,
Complications of tracheostomy can occur intraoperatively and during the early or late gastric distention, dyspnea and aspiration.8 Tracheo-cutaneous stulas occur when a
postoperative periods. The three most common tracheostomy emergencies are the fol- tracheostomy tract becomes completely epithelialized. This can lead to delayed trache-
lowing.8 ostomy closure following decannulation. Tracheo-esophageal and -cutaneous stulas
require surgical intervention.
- Major bleeding
A rare but catastrophic late complication of tracheostomy is tracheo-arterial stula, most
- Tube dislodgment commonly between the trachea and the innominate artery. The incidence is estimated
at 0.6-0.7%, and even when urgently treated only about 20% of patients survive.7 It

is typically a result of direct pressure of the tracheostomy tube against the innominate
artery. Risk factors include low tracheostomy placement and high cuff pressures. 70% Questions
of tracheo-arterial stulas occur within 3 weeks of tracheostomy.7, 8 Emergent interven-
tion - typically surgical, although there are some reports of successful treatment with 15.1 Chronic complications of tracheostomies include all of the following except:
embolization - is required.8 While awaiting denitive intervention, temporizing treat- A. swallowing dysfunction
ment includes occlusion of the stula with tracheal tube pressure - or if unsuccessful, B. tracheomalacia
C. stomal erosion
tube removal and anterior digital pressure. D. innominate artery tracheal stula
E. pneumothorax
15.2 The timing of tracheostomy
Tracheostomy placement is a common surgical procedure encountered in the ICU. A. may impact success of weaning from mechanical ventilation.
Although multiple indications exist, the most common reason is failure to wean from B. is considered late if conducted 10 days after oro-tracheal intubation for respiratory
mechanical ventilation. Unfortunately, at this point in time, no conclusive evidence failure.
exists for early versus late tracheostomy placement in the ICU population. Multiple C. depends on whether an open or a percutaneous tracheostomy is planned.
D. ideally should be on the 4th day following an oro-tracheal intubation for
complications, both early and late, may occur in patients with tracheostomies. As a re- respiratory failure due to pneumonia.
sult, patients should be closely monitored in a critical care setting in the immediate post- E. has no relevance to any patient outcomes.
procedure setting. Not specically discussed in this chapter, tracheostomy weaning,
possible for many patients, occurs via a step-wise management plan and is relatively 15.3 Which of the following is not an indication for tracheostomy?
straightforward. A. a patient with myasthenia gravis unresponsive to medical therapy and has a pH of 7.20
and PaCO2 of 80; the patient has a history of failed oro-tracheal intubation and refuses
awake intubation.
This chapter is a revision of the original chapter authored by Sherif A, MD. B. stridor in a patient with supraglottitis
C. PaCO2 of 62 in a COPD patient with a respiratory rate of 24 on nasal cannula
D. Absence of swallow reex in a patient with a large sub-arachnoid hemorrhage who was
oro-tracheally intubated 7 days ago

15.4 The following are considered emergent complications of tracheostomy tube

placement except:
A. accidental decannulation
B. pneumothorax
C. pneumo-mediastinum
D. swallowing dysfunction
E. stomal hemorrhage

15.5 The most common sequence towards removal of a tracheostomy tube is:
A. weaned mechanical ventilation > vocalization > downsizing > plugging >
B. down-sizing > vocalization > weaned mechanical ventilation > plugging >
C. plugging > decannulation > vocalization > down-sizing > weaned mechanical
D. weaned mechanical ventilation > plugging > downsizing > decannulation >
E. decannulation > downsizing > plugging > vocalization > weaned mechanical

16. Management of Mechanical Ventilation
Daniel W Johnson MD and Edward A Bittner MD PhD

Key Points A 66-year-old man with a history of CAD and COPD is admitted to the ICU
after an open AAA repair. Overnight he remains on full ventilator support
In Assist-Control every breath, whether
(Assist Control, Vt=500 mL, freq=18, FiO2=0.4, PEEP=5). His uid
requirements decrease, and he is hemodynamically stable in the morning.
mandatory or spontaneous, has the same level He has an ABG of pH 7.38 / pCO2 37 / pO2 92 and an actual respiratory
and type of support. rate of 20. He is heavily sedated on propofol and hydromorphone. How
would you proceed towards extubation? Spontaneous breathing trial (SBT)?
Extrinsic PEEP maintains alveolar recruitment, Pressure support ventilation (PSV)? Synchronized intermittent mandatory
increases FRC, decreases pulmonary shunt, ventilation (SIMV)?
may improve lung compliance, and may
decrease the patient work of breathing.

Peak airway pressure is the pressure required

to overcome airway resistance and the elastic
properties of the lung. Whereas, plateau
pressure is an estimate of peak alveolar
pressure, an indicator of alveolar distention.
Mechanical ventilatory support is commonly encountered in the ICU. At present, numerous techniques exist
for the initial control and subsequent support of the respiratory system. A thorough understanding of these
techniques leads to individualized treatment strategies and reduction of complications.

Positive pressure ventilators operate by applying positive pressure (via ow of O2 and/or air) to the airways
during inspiration. In the ICU, mechanical ventilation is almost exclusively positive pressure ventilation.

Negative pressure ventilators create intermittent negative pressure around the thorax and abdomen. The iron
lung, popular during polio outbreaks in the 1940s-50s, is the prototypical example. In modern ICUs, nega-
tive pressure ventilators are almost never used.

Modes of Ventilation
The mode of mechanical ventilation describes the control (volume, pressure, ow, time) and phase variables
(trigger, limit, cycle), which dene how ventilation is provided. The trigger variable is adjusted to sense
patient effort (by negative pressure or by ow at the proximal airway) for the initiation of inspiration. The
limit variable rises no higher than a given preset value or increases to a preset value before inspiration ends.
Cycle is the variable that terminates inspiration (commonly volume, time or ow). Volume Control, Assist Control with Pressure Control, or SIMV with Pressure Control.

Note that in the absence of patient respiratory effort (e.g. in the setting of deep sedation A. Volume Control: A set tidal volume is delivered with a set peak inspiratory ow re-
or neuromuscular weakness or paralysis), there is essentially no difference between the sulting in rising and variable airway pressure during the breath. In SIMV with volume
modes described below: IMV, SIMV and A-C. In the absence of patient effort, these control, only the mandatory breaths are obligated to equal the set tidal volume. In A-C
modes utilize a preset frequency (f) and the preset inspiratory pressure (Pi) or tidal with volume control, all breaths (ventilator initiated and patient triggered) are obligated
volume (Vt) to provide full respiratory support. In other words, the differences between to equal the set tidal volume.
IMV, SIMV and A-C are essentially differences in patient-ventilator interaction.
B. Pressure control: A specic peak airway pressure and an inspiratory time are set.
A. Intermittent mandatory ventilation (IMV): In this mode, the intensivist sets the In order to maintain a constant airway pressure during inspiration, the inspiratory ow
mandatory frequency and tidal volume (if Volume Control) or inspiratory pressure (if waveform is decelerating. The amount of ow necessary to maintain a constant airway
Pressure Control) and the ventilator delivers breaths while allowing the patient to take pressure is affected by the airway resistance and the compliance of the lungs and chest
spontaneous breaths at any time during the respiratory cycle. IMV allows the patient wall. For example, the ventilator might be set at 20 cmH2O for 2 seconds per breath.
to take spontaneous breaths, but all spontaneous breaths are totally unsupported; and This might result in large tidal volumes in patients with compliant lungs and small tidal
IMV has no mechanism for coordinating patient breaths with mandatory breaths. If a volumes in patients with non-compliant lungs.
patient is taking a spontaneous breath when the IMV ventilator is scheduled to give a
mechanical breath, dyssynchrony or breathstacking will occur (the full preset Vt will C. Dual Control (or Adaptive Control) was designed to combine the features of volume
be delivered on top of the patients spontaneous Vt). For example, if the ventilator is set control and pressure control. Vendors use different names to describe this mode of
for IMV with a frequency of 10, the ventilator will initiate a mandatory breath every 6 ventilation: Pressure Regulated Volume Control, Auto-Flow, and Volume Con-
seconds regardless of whether the patient is taking zero or 25 spontaneous breaths per trol Plus are examples of vendor names for dual/adaptive control. In this mode, the
minute. desired tidal volume is set and the ventilator delivers pressure control breaths in order
to achieve the tidal volume. In dual control mode, the ow pattern is initially high and
B. Synchronized IMV (SIMV): This improvement on IMV allows the ventilator to then decelerates just as it is during pressure control mode. The ventilator analyzes the
detect the patients spontaneous breath so that the mandatory mechanical breaths can be delivered tidal volume of the previous breath and adjusts up or down the necessary
delivered in synchrony with spontaneous breaths. SIMV was an improvement on IMV airway pressure to be delivered during the next breath. For example, if the set tidal vol-
because it reduces the risk of dyssynchrony and breath stacking. With early SIMV ume is 500 mL and the current breath has an airway pressure of 15 resulting in an actual
ventilators, spontaneous breaths between mandatory breaths received no support from tidal volume of 420 mL, the ventilator will automatically adjust the airway pressure up
the ventilator. Modern SIMV ventilators can provide varying levels of pressure support on the next breath in an attempt to achieve 500 mL.
(see below) for the breaths between mandatory breaths.
Other modes
If a patient is on SIMV with a mandatory rate of 10, the ventilator will deliver the A. Pressure support (PSV): Unlike IMV or A-C, pressure support does not provide full
mandatory breaths at times when the patient makes an inspiratory effort. If the patient ventilator support to an apneic patient. It is a pressure-preset, ow-cycled mode used
makes no inspiratory effort within a 6 second interval, the mandatory breath will simply to support the patients spontaneous respiratory efforts. With each inspiratory effort
be delivered. the patient triggers the ventilator, which maintains the preset pressure in the circuit
throughout inspiration. The inspiratory cycle ends when the ow rate has decreased to a
C. Assist-control (A-C): In assist-control, every breath, whether it is a mandatory breath pre-determined level (usually 25% of the peak ow rate).
initiated by the ventilator or a patient-triggered breath, receives the same full support
that is prescribed for mandatory breaths. For example, if the A-C ventilator is set at B. Inverse ratio ventilation (IRV): This mode increases the mean airway pressure by
Vt=600mL and freq=8 and the patient makes 30 inspiratory efforts per minute, the venti- prolonging the inspiratory to expiratory (I:E) ratio. The prolonged ination time can
lator will deliver 600mL x 30, or 18 L/min of ventilation. help prevent alveolar collapse, resulting in improved oxygenation. Heavy sedation with
or without neuromuscular blockade is usually required for patients to remain on IRV.

Volume Control, Pressure Control and Dual Control C. Airway pressure release ventilation (APRV): APRV cycles between a high continu-
Independent of the mode (IMV, SIMV, A-C), mechanical ventilation is either volume ous positive airway pressure (HCPAP) and a low continuous positive airway pressure
control (a set tidal volume is delivered during every mandatory breath, resulting in vari- (LCPAP) while allowing the patient to breathe spontaneously at all times. Transition
able airway pressures), pressure control (a set airway pressure is maintained throughout from HCPAP to LCPAP allows deation and transition from LCPAP to HCPAP allows
every mandatory breath, resulting in variable tidal volumes) or dual control (a combina- ination. APRV can improve oxygenation by maximizing alveolar recruitment and
tion of volume and pressure control). This can be confusing for residents in the ICU. reducing shunt.
Remember that a patient can be on Assist Control with Volume Control, SIMV with
D. Proportional assist ventilation (PAV): PAV is synchronized partial ventilatory support
in which the ventilator generates pressure in proportion to the patients instantaneous for variable duration, magnitude and frequency in an effort to recruit atelectatic lung
inspiratory effort. In PAV, the more effort a patient makes, the more support the ventila-
tor provides. PAV was created to more closely mimic the bodys innate communication H. Permissive hypercapnia is an approach to limit ventilator-induced lung injury
between the nervous system and the respiratory system. It is sometimes used in the ICU through deliberate tolerance of elevated PCO2 in the setting of hypoventilation. Contra-
as an alternative to pressure support ventilation. indications include elevated ICP, right ventricular failure, and severe ongoing acidemia.

E. Noninvasive Positive Pressure Ventilation (NPPV): NPPV is the delivery of me- Complications of mechanical ventilation
chanically assisted or generated breaths without an endotracheal or tracheostomy tube.
Ventilation is delivered via face mask, nasal mask or helmet. Advantages of NPPV A. Ventilator-induced lung injury (VILI) occurs when the lung is directly damaged by
include: avoiding the risks of intubation, reduced need for sedation and lower rates of the action of mechanical ventilation. Barotrauma is alveolar overdistention/rupture
healthcare-associated pneumonia. Disadvantages include: lack of protection against related to high inspiratory pressures. Pneumothorax, pneumomediastinum and pneu-
massive aspiration, less airway pressure tolerated, and lack of access to the airways for moperitoneum can occur in this setting. Volutrauma is lung injury from excessive
suctioning. NPPV is most benecial for patients with acute COPD exacerbations and volume rather than excessive pressure. Atelectrauma refers to the possibility of injury
patients with acute cardiogenic pulmonary edema. Other uses include post-extubation to the lung secondary to the cyclic opening and closing of alveoli during mechanical
ventilation. Biotrauma refers to the release of inammatory mediators related to
support, obesity-hypoventilation syndrome, acute post-operative respiratory failure, and mechanical ventilation.
for patients who are not candidates for intubation (DNI order).

1. Continuous positive airway pressure (CPAP): CPAP works by generating a con-

tinuous ow of oxygen and/or air that maintains a continuous positive pressure to the
respiratory system during inspiration and expiration thus preventing airway and alveo-
lar collapse. CPAP may improve alveolar ventilation and oxygenation by reversing
atelectasis, maintaining greater end expiratory lung volume, and preventing obstruction
of the airways.

2. Bi-level positive airway pressure (BiPAP): BiPAP involves independently set inspi-
ratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP).
Vt results from the combination of patient effort and the difference between IPAP and
EPAP. BiPAP can be used as a strategy to reduce PaCO2.

F. Positive end expiratory pressure (PEEP): PEEP may increase oxygenation in lung
diseases characterized by lung collapse.

1. Extrinsic PEEP (PEEP set on the ventilator) is essentially CPAP in between inspira-
tory cycles. It maintains alveolar recruitment, increases FRC, decreases pulmonary
shunt, may improve lung compliance, and may decrease patient work of breathing.
The application of PEEP may have disadvantages: it increases intra-thoracic pressure,
which can decrease venous return and can compromise cardiac output. In addition,
because PEEP has the greatest effect on compliant regions of the lung, over distention Figure 16.1 Ventilator Pressures
can occur, resulting in increased dead space. High levels of PEEP may contribute to
ventilator-induced lung injury (VILI).

2. Intrinsic PEEP or auto-PEEP results from pressure developing from gas trapping B. Oxygen toxicity: Prolonged exposure to high concentrations of oxygen may cause
(dynamic hyperination) due to insufcient expiratory time and/or excessive expira- lung damage. Normal lung units are at highest risk for oxygen toxicity because these
tory airway resistance. Increasing expiratory time, reducing airway resistance, and areas receive the most ventilation. The FiO2 should be reduced when possible provided
reducing minute ventilation (by reducing tidal volume and/or reducing frequency) are that arterial oxygenation is adequate. In adults, an FiO2 of less than 0.5 is considered
methods for reducing auto-PEEP. safe.

G. Recruitment maneuvers refer to the application of elevated pressures and volumes

Mechanics Ppl so that PL can be estimated and ventilator settings adjusted accordingly.
A. Airway pressures (Figure 16.1)
1. Peak (Ppeak) is the pressure reached at end inspiration during positive pressure vol- 3. Work of breathing: To achieve ventilation, work is performed to overcome the
ume control ventilation. Ppeak is the sum of the pressure required to overcome airway elastic and frictional resistances of the lung and chest wall. Work of breathing can be
resistance and the pressure required to overcome the elastic properties of the lung/ calculated by multiplying the change in transpulmonary pressure (PL) times the change
chest. in tidal volume.

2. Plateau (Pplat) reects the pressure required to overcome the elastic properties of the Monitoring and physiology
lung/chest. The Pplat is an estimate of the peak alveolar pressure, which is an indicator A. Oxygenation
of alveolar distention. Measurement of Pplat requires the absence of patient effort and 1. Pulse oximetry is a standard ICU monitor that provides noninvasive measurement of
is obtained during a short inspiratory hold at end inspiration. the oxygen saturation of hemoglobin using differential light absorption characteristics
in oxyhemoglobin versus deoxyhemoglobin. Two wavelengths of light, red (660 nm)
3. Mean pressure is the average pressure within the airway during one complete respi- and infrared (900-940 nm) are passed through a pulsating vascular bed (e.g. a nger-
ratory cycle. It is related to inspiratory time, freq, Ppeak and PEEP. tip) to a photo detector. The relative amounts of red and infrared light reaching the
photo detector provide information about the relative ratio of deoxyhemoglobin and
oxyhemoglobin. These data are compared (by a computer) to calibration curves de-
veloped in studies of healthy volunteers to give an oxygen saturation reading, denoted
B. Compliance is change in volume divided by the change in pressure. SpO2. The actual arterial oxygen saturation, SaO2, correlates well with the SpO2 when
1. Static compliance is measured when airow is absent. It is calculated by Cstat = Vt / the SaO2 is greater than 80%. At lower SaO2 values, the accuracy is diminished. Other
(Pplat -PEEP). When airow is absent, the airways resistance is not a factor. Thus static causes of inaccurate SpO2 include dyshemoglobinemias, dyes, pigments, low perfu-
compliance reects the distensibility of the lung/chest only. sion, motion, abnormal pulse, extreme anemia and external light sources.

2. Dynamic compliance is measured when airow is present at end inspiration. Since 2. Arterial blood gas (ABG) analysis provides (among other data) a measurement of
airow is present, airways resistance contributes to Cdyn. It is calculated by Cdyn = Vt / the partial pressure of oxygen (PaO2), which represents the amount of oxygen dis-
(Ppeak-PEEP) solved in arterial blood. It is important to remember that dissolved oxygen (represent-
ed by PaO2) makes up a small portion of the total arterial oxygen content. The oxygen
3. Comparing static and dynamic compliance can help identify the cause(s) for dif- content of arterial blood (CaO2) consists of two components: oxygen bound to hemo-
culty with ventilation or difculty with discontinuing the ventilator. Cdyn is decreased globin (which determines the SaO2) and the oxygen dissolved in plasma (which deter-
by conditions where airways resistance is increased (e.g. bronchospasm), while the Cstat mines the PaO2). CaO2 is described by CaO2 =[1.34 * Hgb * SaO2] + [PaO2 * 0.003]
is unaffected by such conditions. where 1.34 mL O2 per gram Hgb is a constant, Hgb is hemoglobin in g/dL, SaO2 is the
arterial oxygen saturation and should be in decimal form (e.g. 98% is written 0.98),
PaO2 is in mmHg, and 0.003 mL O2 per mmHg per dL is a constant
4. Resistance (R) is the change in pressure divided by the ow. It is calculated by R =
(Ppeak Pplat) / F where F is the peak inspiratory ow rate
a) Intermittent ABG: A sample of arterial blood is inserted into a blood gas analyzer
intermittently and results are displayed within a few minutes
C. Pressure- ow relationships
1. Flow of air into the alveolus is driven by trans-pulmonary pressure (PL), or the b) Continuous ABG monitors detect variations in light and uorescence to allow the
difference between alveolar pressure and pleural pressure. PL is calculated by PL = PA continuous display of ABG results. These monitors are subject to a variety of arti-
- Ppl. PL is transpulmonary pressure; PA is alveolar pressure; and Ppl is pleural pressure. facts and are not routinely used in the ICU.
Flow, transpulmonary pressure and resistance relationships are summarized by Flow =
PL / R, where PL = PA - Ppl Because PA and Ppl are difcult to measure directly, they are
estimated by Pplat and esophageal pressure (Pes) respectively in clinical practice. Hence, 3. Transcutaneous oxygen tension monitoring uses the polarographic principle to mea-
Flow = (Pplat- Pes)/R. sure PO2 at a warmed skin surface. This monitor is particularly useful in neonates and
infants, but due to technical and physiologic limitations in adult patients, it is rarely
used in the adult ICU.
2. Esophageal pressure changes reect pleural pressure changes (the absolute Pes does
not reect absolute pleural pressure). Pes is measured with a thin walled balloon in the
lower esophagus. Changes in Pes can be used to assess chest wall compliance during 4. The shunt fraction is the proportion of the cardiac output that does not participate
full ventilator support and to assess respiratory effort, work of breathing and auto- in gas exchange. Normal shunt fraction is approximately 3-8% and is mostly due to
PEEP during spontaneous breathing and patient-triggered modes of ventilation. In se- the bronchial circulation. The degree of shunt can be estimated by the shunt equation:
vere lung disease (e.g. severe ARDS), esophageal manometers can be used to estimate Qs/Qt = (CcO2 CaO2) / (CcO2 CvO2) where Qs is shunt, Qt is total cardiac output,

CcO2is end-capillary O2 content, CaO2 is arterial O2 content and CvO2 is mixed venous cardiac output. Administration of intravascular uid may counteract the negative hemo-
O2 content dynamic effects of positive pressure ventilation.

5. Global oxygen delivery (DO2) is the product of arterial O2 content and the cardiac B. Afterload reduction: Lung expansion increases extramural pressure, which helps
output: DO2 = CaO2 * CO * 10 where DO2 is in mL/min, CaO2 is in mL/dL, CO is to pump blood out of the thorax and thereby reduce LV afterload. In conditions where
cardiac output in L/min, and 10 converts L into dL. cardiac function is mainly determined by changes in afterload rather than preload (e.g.
hypervolemic patient with systolic heart failure), positive pressure ventilation may be
6. Oxygen consumption (VO2) is calculated by the Fick equation VO2 = CO * (CaO2 associated with improved cardiac output.
CvO2) where VO2 and CO are in L/min.
C. Shunt effects: In patients with right-to-left intra-cardiac shunts, positive pressure
B. Ventilation ventilation and PEEP may increase right-to-left shunt and worsen systemic hypoxemia.
The mechanism of increased shunt is likely Valsalva-like activity (e.g. breathing against
1. Capnometry/capnography: The capnometer is a device that measures CO2 in ex- the ventilator) or an increase in pulmonary vascular resistance secondary to PEEP.
haled gas and the capnograph provides a display and ability to track changes in CO2.
Quantitative capnometers measure CO2 using infrared spectroscopy, Raman spectros-
copy or mass spectroscopy. Quantitative capnometers and capnography are standard
monitors in the operating room and can be used in the ICU to non-invasively estimate/ Miscellaneous
track the PaCO2. In the setting of lung disease, capnometry is less accurate in its esti- A. Hyperbaric oxygen (HBO, HBOT) therapy involves breathing 100% oxygen at > 1
mate of PaCO2. Non-quantitative capnometers indicate the presence of CO2 by color atmosphere of pressure. HBOT is administered in specialized chambers under close
change of an indicator material (e.g. for conrmation of endotracheal tube placement). patient monitoring. Mechanisms of action of HBO therapy stem from 2 types of effects:
hyperoxygenation of perfused tissues and reduction of gas bubble volume. Indications
2. ABG: the arterial partial pressure of CO2 reects the balance between CO2 produc- include:
tion and the alveolar ventilation. PaCO2 varies directly with CO2 production (VCO2) 1. Air embolism: The effect of HBO is predicted by Boyles Law, which states that
and inversely with alveolar ventilation (VA) as described by: PaCO2 = VCO2 / VA. the volume of air (mostly nitrogen) bubbles is inversely proportional to the pressure
Minute ventilation (VE) affects the PaCO2 only to the extent that it affects the alveolar exerted on them. Nitrogen bubble size is further reduced by replacement of nitrogen
ventilation (VA). with oxygen, which is rapidly used in cellular metabolism. Air embolism can result
from procedures (e.g. central line placement) or operations (e.g. sitting craniotomy) in
3. CO2 production is a function of O2 consumption and CO2 that is liberated in the which air can be entrained through a disrupted vascular wall.
buffering of H+ ions. In normal physiology, increased CO2 production is rapidly fol-
lowed by an increase in alveolar ventilation to eliminate excess CO2 and maintain 2. Decompression sickness (the bends): Divers breathing compressed air who return
normal PaCO2. In patients with impaired ability to increase alveolar ventilation (e.g. to the surface too rapidly are at risk for decompression sickness, which occurs when
sedation, weakness or lung disease), an increase in CO2 production can result in an bubble formation in blood and tissues occurs as the partial pressure of inert gas (ni-
increase in PaCO2. Overfeeding is a recognized cause of hypercapnia in patients with trogen) exceeds that of ambient air. HBO is the primary treatment for decompression
respiratory failure. Overfeeding with carbohydrates is especially problematic because sickness through its effects on bubble size and relief of hypoxia.
metabolism of carbohydrates generates more CO2 than do lipids or proteins.
3. Carbon monoxide (CO) poisoning: HBO signicantly reduces the half-life of car-
4. Dead space (Vd) refers to ventilation that does not participate in gas exchange. The boxyhemoglobin, which may prevent the late neurocognitive defects associated with
dead space ratio is calculated from the Bohr equation which measures the ratio of severe CO poisoning.
dead space to tidal volume: Vd / Vt = (PaCO2 PeCO2) / PaCO2 where PeCO2 is the
CO2 concentration in mixed expired gas, NOT end-tidal CO2, though end-tidal CO2 4. Soft tissue infections: HBO has been used as an adjunct therapy for severe life or
is sometimes used as an estimate. The normal dead space to tidal volume ratio is 0.3 limb threatening infections such as clostridial myonecrosis, necrotizing fasciitis and
to 0.4. High dead space ratio can be predictive of failure to successfully discontinue Fourniers gangrene.
mechanical ventilation.
B. Independent lung ventilation (ILV): Patients with severe unilateral lung disease may
5. Transcutaneous CO2 monitoring has been used in the neonatal ICU but has had require different ventilation strategies applied to each lung. Indications for indepen-
limited acceptance in the adult ICU. dent lung ventilation include: unilateral pulmonary contusion, bronchopleural stula,
massive hemoptysis from a single lung, or following single lung transplantation (though
Cardiopulmonary interactions ILV is not routinely used for any of these conditions). A double lumen tube and two
A. Venous return: Administration of positive pressure ventilation causes increased
intrathoracic pressure, which can cause decreased venous return leading to reduction in
ventilators facilitate ILV. REFERENCES
1. Bigatello LM ed: Critical Care Handbook of the Massachusetts General Hospital, 5th
Ed. Philadelphia, Lippincott Williams & Wilkins, 2010.
C. Heliox is a gas mixture of helium and oxygen that is used in conditions of high 2. Fink MP, Abraham E, Vincent JL and Kochanek P eds: Textbook of Critical Care, 5th
airow resistance. Helium is less dense than air and ows more readily through regions Ed. Philadelphia, Elsevier Saunders, 2005.
of reduced cross-sectional area where ow is turbulent. (Turbulent ow is dependent on 3. Hess D, MacIntyre NR, Mishoe SC et al eds: Respiratory Care: Principles and Practice.
the uid or substances density. This is in contrast to laminar ow, which is dependent Philadelphia, WB Saunders, 2002.
4. Marino PL. The ICU Book, 3rd Ed. Philadelphia, Lippincott Williams & Wilkins, 2007.
on viscosity). Heliox may be useful in acute exacerbations of asthma / COPD or in 5. McLean B and Zimmerman JL eds: Fundamental Critical Care Support, 4th Ed. Soci-
tracheal obstruction. Heliox is generally well tolerated but its use is frequently limited ety of Critical Care Medicine, Mount Prospect, IL, 2007.
by the high concentration of helium required, which limits FiO2 delivery. Most studies 6. Irwin RS and Rippe JM eds: Intensive Care Medicine, 6th Ed. Philadelphia, Lippincott
use a helium:oxygen mixture of 80:20 or 70:30 to achieve benet. Many ICU patients Williams & Wilkins 2008.
can not tolerate an FiO2 of 0.2 or 0.3 due to hypoxemia.

D. High frequency ventilation achieves gas exchange by combining very high respira-
tory rates with very low tidal volumes (smaller than anatomic dead space). Potential
advantages include a lower risk of barotrauma due to small tidal volumes and improved
gas exchange due to more uniform distribution of ventilation and greater alveolar re-
1. High frequency jet ventilation (HFJV) delivers pulses of gas at high velocity and 16.1 Static compliance will be independently affected by:
frequency into the trachea through a small catheter. The high velocity jet pulse creates A. Pulmonary edema
an area of reduced pressure, which entrains additional gas and produces a mixing ef- B. Bronchospasm
C. Kinked endotracheal tube
fect. Exhalation is a passive process. HFJV has been used in ARDS patients with the D. Mucus plugging
goal of reducing airway pressures and ventilator induced lung injury.
16.2 Goals of adding PEEP to routine ventilation settings might include all of the following
2. High frequency oscillatory ventilation (HFOV) delivers low tidal volumes at very EXCEPT:
A. Improved lung compliance
high frequency using a pump so that airway pressure oscillates slightly about a mean B. Improved PaO2
airway pressure. This allows maintenance of alveolar recruitment while avoiding high C. Decreased work of breathing
peak airway pressure. HFOV has been used primarily in children and neonates where D. Reduced dead space
its use is associated with improved oxygenation and reduced barotrauma.
16.3 A contraindication to permissive hypercapnia is:
A. Hypoxia
Future directions B. Plateau pressure > 25 cm H2O
A. Improvement in ventilator technology has allowed for the recent development of a C. Brain injury with very high intra-cranial pressures
variety of modes (e.g. Neurally Adjusted Ventilatory Assist, or NAVA) with increased
emphasis on patient ventilator interactions. The goal is to mimic the complex interplay
of the central nervous system, peripheral nervous system and respiratory system exhib-
ited during normal breathing.

B. Alternatives to traditional positive pressure mechanical ventilation, including

pumpless extracorporeal gas-exchange devices driven by the patients blood pressure,
continue to attract more attention as intensivists seek to minimize ventilator induced
lung injury.

Proper management of mechanical ventilation requires a thorough understand-
ing of respiratory and cardiovascular physiology and pathophysiology of critical illness.
While a wide variety of ventilator modes exist, the recovery of patients in respiratory
failure depends mostly on clinicians vigilance and ability to modify therapy appropri-

17. Weaning from Mechanical Ventilation
Jarett Skirball MD and Peter M Schulman MD

Key Points A 73 year-old man was admitted to the ICU for aspiration pneumonia.
Over the next 36 hours, he developed worsening hypoxic respiratory failure
Prolonged mechanical ventilation is
requiring non-invasive bilevel positive airway pressure, and ultimately
intubation and mechanical ventilation. )n volume-assist control ventilation
associated with adverse outcomes such as (AC) with a tidal volume of 6 ml/kg based on predicted ideal body weight,
higher rates of pneumonia, longer intensive he required a FiO2 of 0.7 with PEEP of 12 cmH2O to maintain a SpO2 greater
care unit stays, and increased mortality. than 90%.
On ICU day 5, his sedation was discontinued but he remained minimally
The weaning process constitutes a significant responsive. Ventilator settings were AC, FiO2 0.4 PEEP 8. Hemodynamic
proportion of time critically ill patients spend indices were stable. He was noted to gag and cough with endotracheal
receiving mechanical ventilation. suctioning and had minimal respiratory secretions. An ABG demonstrated
pH 7.33/PaCO2 52/PaO2 80. He was then placed on a spontaneous
A proactive approach to ventilator weaning breathing trial with pressure support 5 cmH2O and PEEP 5 cmH2O.
is critical. Clinicians should make a daily However, after 17 minutes, his breathing became more labored and his RR
determination of weaning readiness, initiate
increased from 22 to 37.
the weaning process as soon as predetermined
criteria are met, and liberate patients from
mechanical ventilation as quickly as possible. Introduction
In the United States, approximately 800,000 patients per year require mechanical ventilation (MV).1 When
Protocol directed weaning strategies with prolonged, MV is associated with adverse outcomes such as higher rates of pneumonia, longer intensive care
daily spontaneous breathing trials shorten the unit (ICU) and hospital stays, and increased mortality.2
duration of mechanical ventilation.
Weaning is the process of liberating a patient from MV. It encompasses a continuum of care that starts once
the underlying cause for intubation has been addressed. It involves improving the strength-to-load ratio of the
Weaning failure should prompt a thorough respiratory system by stepping down the level of mechanical support and encouraging spontaneous breath-
evaluation for potentially reversible causes. ing prior to extubation.1 For the majority of patients, this process is uncomplicated and can be accomplished
expeditiously (e.g. routine postoperative extubation). However, in the setting of acute or chronic respiratory
failure, minimizing the duration of MV is an important goal. Evidence based strategies to improve outcomes
and reduce the duration of MV include small tidal volume ventilation in patients with or at risk for acute
respiratory distress syndrome, daily interruption of sedatives or the avoidance of sedatives altogether, early
physical and occupational therapy, conservative uid management, and the prevention of ventilator associated

In terms of reducing the duration of MV, shortening the weaning process is another key consideration, as
weaning accounts for an average of 40-50% of the time spent receiving MV.3 It is therefore critical to contin-
uously assess readiness for weaning, start the weaning process as soon as is appropriate, liberate patients from
mechanical ventilation as soon as extubation criteria are met, and take steps to prevent reintubation whenever
possible. A proactive, protocol driven, evidence-based approach to the weaning process
will dramatically shorten the duration of mechanical ventilation and improve outcomes.

Categorizing the Weaning Process

Different classication systems have been proposed to categorize the weaning process
based on its duration and the number of spontaneous breathing trials (SBT) required, as
well as to assist clinicians in risk stratifying mechanically ventilated patients. One such
system, developed by an international task force in 2007, is as follows:7
- Simple: Patients who are successfully extubated following a rst attempt
(approximately 60% of ICU patients).8
- Difcult: Patients who fail initial weaning and require up to three SBTs or up
to seven days for successful extubation (approximately 25% of ICU patients and
associated with increased morbidity).8
- Prolonged: Patients who fail three or more weaning attempts or require seven or
more days of MV (approximately 15% of ICU patients and associated with increased
hospital mortality).8

Weaning Readiness
In any mechanically ventilated patient, daily assessment for weaning readiness should Figure 17.1 Algorithm for Weaning from Mechanical Ventilation
SBT: spontaneous breathing trial; MV: mechanical ventilation.
be immediately initiated once the inciting respiratory insult has begun to improve.1 The Adapted from Figure 1 in McConville and Kress1.
effects of any neuromuscular blocking agents must be reversed and sedatives that sup-
press the respiratory drive should be sufciently weaned or held.9 progressively longer durations. PS was found to signicantly reduce the duration of
Other prerequisites for weaning readiness include:7
- Stable hemodynamics (the patient should be on little to no vasoactive support, or at Esteban et al. enrolled patients who had initially failed a breathing trial into one of four
a minimum, this requirement should be decreasing or stable) weaning strategies: 1) SIMV with gradual reduction in backup rate; 2) PS ventilation in
- Sufcient respiratory muscle strength and pulmonary function (the patient should which the pressure support was gradually decreased; 3) multiple daily T-piece trials; or
be able to sustain spontaneous breathing and maintain acceptable gas exchange with 4) once per day T-piece trials. These authors found that the once daily versus multiple
vital capacity > 10 ml/kg, respiratory rate < 35 breaths/min., negative inspiratory force daily T-piece trials were equivalent, and that both approaches were superior to either
< -20 cm H2O, tidal volume > 5ml/kg) SIMV or PS.6
- Acceptable oxygenation (SpO2 >90% on FiO2 < 0.4 PEEP < 8 cmH2O, or
PaO2:FiO2 ratio > 150) Based on evidence from these and other studies, expert consensus is that 1) intermittent
- Optimized volume status (euvolemia or net negative uid balance) trials of spontaneous breathing via T-piece or PS are likely equivalent, and 2) evidence
- Acceptable electrolyte prole (potassium, calcium, and phosphate are important for clearly does not favor the use of SIMV for weaning.7
muscle function)
- Adequate mentation (mental status must at least be sufcient to cooperate with the Attempts have been made to wean patients from MV using alternative (or newer) modes
weaning process, however a low Glasgow Coma Score is not necessarily, in and of of ventilation with limited success. A noteworthy example is automatic tube compen-
itself, a contraindication to weaning or extubation) sation (ATC). This mode, which has a unique ability to compensate for the nonlinear
pressure drop across the endotracheal tube (ETT) during spontaneous breathing, was
found to be equally as efcacious as a T-piece or PS for weaning in at least one study.10
Evidence Based Weaning Strategies Although consideration should be given to ATC for patients who fail a SBT because of
The efcacy of different weaning modes has been evaluated in prospective randomized a small diameter ETT, there is a lack of evidence to make denite statements about the
studies. use of ATC for difcult to wean patients.7

Out of 456 mechanically ventilated patients, Brochard et al. randomized 109 patients The Weaning Process / Spontaneous Breathing Trial
who had initially failed a breathing trial to one of three weaning strategies: 1) gradual
reduction in pressure support (PS); 2) synchronized intermittent mandatory ventila- Neither clinical experience alone nor complex algorithms have been shown to accurate-
tion (SIMV) with gradual reduction in backup rate; or 3) intermittent T-piece trials of ly predict whether mechanically ventilated patients can breath spontaneously. Rather,
the denitive test or gold standard to gauge a patients readiness for spontaneous
breathing is the spontaneous breathing trial (SBT).1 A SBT is performed with little to respiratory capacity. Considerations include an unresolved primary insult, excessive
no ventilatory support; it is accomplished by switching from a mode that provides full work of breathing due to other disease processes, air trapping (autopeep), etc.]
support such as AC to either PS or continuous positive airway pressure (CPAP). Alter- 3) Cardiovascular (myocardial ischemia, left or right ventricular failure; weaning
natively the patient can be placed on T-piece. Ideally, sedative infusions that suppress can increase myocardial wall stress, increase myocardial demand and unmask
respiratory drive and level of consciousness should be held.1 myocardial dysfunction)
Esteban conducted a multicenter prospective randomized controlled trial in 526 med- 4) Neurologic or Neuromuscular (cerebral hemorrhage or ischemia, critical illness
ical-surgical ICU patients to determine the effect of SBT duration on outcome. They myopathy or neuropathy)
found after a rst SBT, whether targeted to 30 minutes or 120 minutes in duration, were 5) Nutrition (malnutrition or overfeeding)
equally efcacious at achieving successful extubation.11 Most practioners today believe
a SBT lasting 30 minutes is generally sufcient. 6) Electrolytes (hypomagnesemia, hypophosphatemia)
The SBT is a binary test in which failure can be dened by objective and subjective 7) Acid Base (metabolic alkalosis, acidosis)
parameters such as the following:1 8) Infection
1) Respiratory rate > 35 breaths per minute for more than 5 minutes Rates of extubation failure vary widely among ICUs. On average, approximately 15%
2) Oxygen saturation of < 90% of patients in whom mechanical ventilation is discontinued require reintubation within
48 hours.7 The average rate of failed extubations in surgical ICUs is 5-8% while in
3) Heart rate > 140 beats per minute or sustained change in HR of > 20% medical and neurologic ICUs it is as high as 17%. Non-invasive ventilation to prevent
4) Systolic blood pressure of > 180 mm Hg or < 90 mm Hg re-intubation may be benecial when ventilation, but not oxygenation, is the cause of
5) Anxiety failure. Reintubation is associated with prolonged hospital stay and increased mortal-
6) Diaphoresis ity.1

Aside from the SBT, other methods to predict readiness for spontaneous breathing Tracheotomy may be considered for patients who require prolonged weaning. Ratio-
and extubation have been proposed and evaluated. Yang and Tobin found the ratio of nale for early tracheotomy includes easier airway suctioning, improved patient comfort
respiratory rate (in breaths per minute) to tidal volume (in liters), termed rapid shallow with less sedation and enhanced ability to communicate (decreased requirement for
breathing index (RSBI), to be a useful adjunct to the SBT. Specically, a RSBI > 105 sedatives). However, the timing of tracheotomy remains controversial.1 A recent meta
was found to accurately predict extubation failure, however a RSBI < 105 was not as analysis concluded that there is insufcient evidence of improved outcomes to warrant a
accurate at predicting patients who could be successfully extubated. These ndings have recommendation for early tracheotomy.15
been subsequently corroborated by a systematic review of multiple RSBI studies.12
Failure to wean from mechanical ventilation should promptly initiate a thorough and
Many studies have demonstrated that developing and instituting a protocol driven systematic search for the underlying etiology, as often times, the patients condition can
approach to weaning is benecial. Benets include a decreased time to extubation3, be further optimized and/or the underlying cause for failure is potentially reversible.
possible decrease in the incidence of reintubation, and in at least one study, a decrease
in the incidence of ventilator associated pneumonia and mortality.13 Additionally, pair- Summary
ing SBTs with a sedation holiday may improve extubation success and mortality.14 A Mechanically ventilated patients should be assessed at least daily for weaning readi-
protocolized approach to weaning should ideally be developed in a multidisciplinary ness. Patients who meet criteria should be promptly placed on a SBT. In general, a
fashion, and once implemented, these protocols can often be performed by nurses or SBT should be targeted to 30 minutes duration and should be performed by placing the
respiratory therapists.1 patient on low-level PS or a T-piece. Patients passing a SBT should immediately be
assessed for extubation and liberated from the ventilator, if appropriate. Failure to wean
Final considerations following a successful SBT and prior to extubation are to ensure at any stage should prompt a search for an etiology, and reversible causes of failure
the patient can maintain a patent airway. There should be an assessment of the quan- should be corrected or at least further optimized. In the interim, a non-fatiguing form
tity and consistency of secretions, presence of a strong enough cough, an adequate gag of MV should be utilized. See Figure 17.1 for an algorithm summarizing the weaning
reex and/or swallow, and, if appropriate, verication of an adequate endotracheal tube process.
cuff leak.7 Mental status is also a key component regarding the patients ability to pro- A proactive, standardized, and evidence-based approach to weaning reduces the dura-
tect his/her airway. tion of MV and improves outcomes. Best practice in the ICU should incorporate a
structured and evidence-based approach to weaning from MV.
Prolonged Weaning and Weaning Failure
Weaning failure occurs when a SBT is not successful or a patient requires reintubation
within 48 hours of extubation.7 In assessing reasons for weaning failure, it may be help- References:
ful to take a systems based approach: 1. McConville JF, Kress JP: Weaning Patients from the Ventilator. N Engl J Med 2012;
1) Fatigue (weaning to exhaustion) 2. Coplin WM, Pierson DJ, Cooley KD, Newell DW, Rubenfeld GD: Implications of extuba-
2) Respiratory [The primary issue is an imbalance between the respiratory load and tion delay in brain-injured patients meeting standard weaning criteria. Am J Respir Crit

Care Med 2000; 161:1530-6
3. Ely EW, Baker AM, Dunagan DP, Burke HL, Smith AC, Kelly PT, Johnson MM, Questions
Browder RW, Bowton DL, Haponik EF: Effect on the duration of mechanical ventilation of
identifying patients capable of breathing spontaneously. N Engl J Med 1996; 335:1864-9
4. Blackwood B, Alderdice F, Burns KE, Cardwell CR, Lavery G, OHalloran P: Proto- 17.1 In reference to the case description at the beginning of this chapter, what is the next best
colized versus non-protocolized weaning for reducing the duration of mechanical ventila- step in his management?
tion in critically ill adult patients. Cochrane Database Syst Rev 2010; (5):CD006904 A. Proceed directly to extubation
5. Brochard L, Rauss A, Benito S, Conti G, Mancebo J, Rekik N, Gasparetto A, Lemaire B. Place the patient back on AC for 24 hours, then attempt another SBT
F: Comparison of three methods of gradual withdrawal from ventilatory support during C. Switch to synchronized intermittent mandatory ventilation (SIMV) with pressure support
weaning from mechanical ventilation. Am J Respir Crit Care Med 1994; 150:896-903 and gradually decrease pressure support as tolerated.
6. Esteban A, Frutos F, Tobin MJ, Alia I, Solsona JF, Valverd I, Fernndez R, de la Cal
MA, Benito S, Toms R, et al: A comparison of four methods of weaning patients from 17.2 In reference to the case description at the beginning of this chapter, which of the following
mechanical ventilation. Spanish Lung Failure Collaborative Group. N Engl J Med 1995; should be further optimized prior to extubation?
332:345-50 A. Low Glasgow Coma Score
7. Boles JM, Bion J, Connors A, Herridge M, Marsh B, Melot C, Pearl R, Silverman H, B. Malnutrition
Stanchina M, Vieillard-Baron A, Welte T: Weaning from mechanical ventilation. Eur Respir C. Chest radiograph demonstrating large right sided pleural effusion
J 2007; 29:1033-56
8. Funk GC, Anders S, Breyer MK, Burghuber OC, Edelmann G, Heindl W, Hinterholzer 17.3 Which of the following is not an evidence-based indication for the use of non-invasive
G, Kohansal R, Schuster R, Schwarzmaier-DAssie A, Valentin A, Hartl S: Incidence and ventilation?
outcome of weaning from mechanical ventilation according to new categories. Eur Respir A. Preventing reintubation of a patient with a PaCO2 of 70 mmHg and SpO2 93% on 2L
J 2010; 35:88-94 nasal cannula shortly after extubation.
9. Kress JP, Pohlman AS, OConnor MF, Hall JB: Daily interruption of sedative infusions B. Preventing reintubation of a patient with a PaCO2 of 40 mmHg and SpO2 88% on FiO2
in critically ill patients undergoing mechanical ventilation. N Engl J Med 2000; 342:1471- 0.9 shortly after extubation
7 C. Preventing reintubation of a patient with a COPD exacerbation
10. Haberthr C, Mols G, Elsasser S, Bingisser R, Stocker R, Guttmann J: Extubation
after breathing trials with automatic tube compensation, T-tube, or pressure support
ventilation. Acta anaesthesiol Scand 2002; 46:973-9
11. Esteban A, Ala I, Tobin MJ, Gil A, Gordo F, Vallverd I, Blanch L, Bonet A, Vzquez A,
de Pablo R, Torres A, de La Cal MA, Macas S: Effect of spontaneous breathing trial dura-
tion on outcome of attempts to discontinue mechanical ventilation. Spanish Lung Failure
Collaborative Group. Am J Respir Crit Care Med 1999;159:512-8
12. Meade M, Guyatt G, Cook D, Grifth L, Sinuff T, Kergl C, Mancebo J, Esteban A,
Epstein S: Predicting success in weaning from mechanical ventilation. Chest 2001;
13. Dries DJ, McGonigal MD, Malian MS, Bor BJ, Sullivan C: Protocol-Driven Ventilator
Weaning Reduces Use of Mechanical Ventilation, Rate of Early Reintubation, and Ventila-
tor-Associated Pneumonia. J Trauma 2004; 56:943-52
14. Girard TD, Kress JP, Fuchs BD, Thomason JW, Schweickert WD, Pun BT, Taichman
DB, Dunn JG, Pohlman AS, Kinniry PA, Jackson JC, Canonico AE, Light RW, Shintani
AK, Thompson JL, Gordon SM, Hall JB, Dittus RS, Bernard GR, Ely EW: Efcacy and
safety of a paired sedation and ventilator weaning protocol for mechanically ventilated
patients in intensive care (Awakening and Breathing Controlled trial): a randomised con-
trolled trial. Lancet 2008; 371:126-34
15. Gomes Silva BN, Andriolo RB, Saconato H, Atallah AN, Valente O: Early versus late
tracheostomy for critically ill patients. Cochrane Database Syst Rev 2012; 3:CD007271
16. Vallverd I, Calaf N, Subirana M, Net A, Benito S, Mancebo J. Clinical characteristics,
respiratory functional parameters, and outcome of a two-hour T-piece trial in patients
weaning from mechanical ventilation. Am J Respir Crit Care Med 1998; 158:1855-62
17. Esteban A, Frutos-Vivar F, Ferguson ND, Arabi Y, Apeztegua C, Gonzlez M, Ep-
stein SK, Hill NS, Nava S, Soares MA, DEmpaire G, Ala I, Anzueto A: Noninvasive
positive-pressure ventilation for respiratory failure after extubation. N Engl J Med 2004;
18. Ferrer M, Valencia M, Nicolas JM, Bernadich O, Badia JR, Torres A: Early Noninvasive
Ventilation Averts Extubation Failure in Patients at Risk: a randomised trial. Am J Respir
Crit Care Med 2006; 173:164-70

Section 5: Shock and Cardiac Management


Management of Shock

Diagnosis and Treatment of


Diagnosis and Treatment of Myocardial


Valvular Heart Disease

Adult Congenital Heart Disease

Extra-Corporeal Life Support and

Ventricular Assist Devices

18. Management of Shock
David P Ciceri MD

Key Points A 65 year old female initially is admitted to the hospital with abdominal
pain and fever. A CT scan showed right lower quadrant mass and she is
Hypovolemic, cardiogenic, obstructive and
found to have an abscess at laparotomy. She has a very slow recovery
on the hospital ward. 9 days after surgery she developed a deep venous
distributive are the four classic categories of thrombosis of her left upper extremity secondary to a PICC line and was
shock. therapeutically anticoagulated with heparin. Two days later she developed
a depressed level of consciousness, heart rate of 115 beats per minute and
Patients in shock commonly have a a systolic blood pressure of 84 mm Hg, and was transferred to the ICU.
combination of types of shock. Immediately upon arrival in the ICU, the patient had a large melanic stool,
heart rate increased to 135 and systolic blood pressure fell to 65 mm Hg.
Dynamic parameters, rather than static
parameters, have been demonstrated to be
highly predictive of fluid responsiveness in
hypotensive patients.

Trauma patients in hemorrhagic shock should

be resuscitated with PRBC and FFP in a 1:1 ratio
and consideration to including platelets also in Overview
a 1:1:1 ratio. Shock is a clinical syndrome characterized by inadequate perfusion to meet organ and/or cellular needs. The
adequacy of perfusion is commonly described in terms of oxygen delivery, which is the product of cardiac
Hydroxyethyl starch solutions should not be output and arterial oxygen content. The principal components of arterial oxygen content are the hemoglobin
and arterial oxygen saturation. Shock may be caused by a signicant decrease in oxygen delivery or less
given to critically ill patients including those commonly a relative inability of oxygen delivery to meet increased oxygen or perfusion demands. Shock may
with sepsis, and those admitted to the ICU. also be caused by the loss of the microcirculation to appropriately direct perfusion to areas of cellular need as
is commonly seen in distributive shock states. Lastly, there may be impaired utilization of oxygen at the cel-
lular level. Some investigators hypothesize this occurs with mitochondrial dysfunction in septic shock. Also,
more than one physiological abnormality can be contributing to shock in a given patient.

Types of shock
A common approach to categorizing different types of shock states is into four separate shock syndromes:
A. Hypovolemic
B. Cardiogenic
1. Left ventricular systolic dysfunction most common in adults
2. Dysrhythmmias
3. Valvular disease
4. Right ventricular failure
5. Hypertrophic cardiomyopathy Renal:
C. Obstructive shock A. Decreased urine output
1. Massive pulmonary embolism
2. Cardiac tamponade Common laboratory ndings:
3. Tension pneumothorax A. Hypoxemia
D. Distributive or vasodilated shock B. Metabolic acidosis
1. Septic shock C. Increased serum lactate
2. Neurogenic shock secondary to spinal cord injury D. Elevated troponin with myocardial ischemia but mild to moderate elevations can
3. Acute adrenal insufciency also be seen secondary to myocardial dysfunction in septic shock
4. Hepatic failure E. Coagulation abnormalities and thrombocytopenia
5. Anaphylactic shock F. ECG ndings suggestive of myocardial ischemia or infarction in cardiogenic
shock. Non-specic abnormalities common in other shock states.
This classic description is useful but also a signicant over simplication, which may G. CXR
lead to improper management on occasion. First, complicated patients may have more 1. Cardiogenic pulmonary edema
than one etiology of shock and the clinician must rapidly search for additional diagnoses 2. ARDS
especially if the patient is responding poorly to efforts at resuscitation. Second, all se-
vere hypoperfusion/ shock states, if uncorrected, will ultimately lead to systemic inam-
mation and the superimposition of a distributive or vasodilated shock state. Lastly, this Monitoring in patients with shock
classication system may lead to an under appreciation of the complex changes which To borrow a phrase from Stephen King, the world of monitoring has moved on in most
are commonly present in patients with severe septic shock. There will be signicant intensive care settings. Pulmonary artery catheterization (PAC) is rarely performed in
vasodilation of both the venous capacitance vessels, as well as the arteriolar resistance any setting outside of cardiac surgery in most institutions. There are probably specic
vessels, leading to signicant relative hypovolemia until volume resuscitation restores clinical scenarios (i.e. patient with pulmonary hypertension and severe right ventricular
an adequate intravascular volume. There is increased movement of all acellular uids dysfunction) in which the information obtained from a pulmonary artery catheter can be
into the interstitium so that the patient will need continued volume therapy until inam- essential to guide therapy. One result of the dramatic decline in the use of pulmonary
mation begins to abate. In addition, in adults with septic shock there is invariably bi- artery catheters is the loss of physician and nursing expertise in the use of this monitor-
ventricular systolic and diastolic dysfunction. The myocardial dysfunction may be mild ing device in complicated patients outside of the Cardiac Surgery Intensive Care Unit.
and the patient may have an elevated cardiac output after volume resuscitation because The reduced expertise and the decreased data quality may increase complications.
of tachycardia and a decreased afterload because of vasodilation. But in a signicant
number of patients (> 1/3) the myocardial depression will be more severe and the pa- A second major shift has been the realization that static lling pressures such as the
tient will have a low normal or even low cardiac output despite optimal resuscitation. central venous pressure (CVP) and the pulmonary capillary wedge pressure (PCWP)
have questionable value in assessing volume status, preload or predicting uid respon-
Assuming good cardiac function in an adult with septic shock is a common potentially siveness in any ICU patient population. Dynamic parameters, however, have been
lethal mistake. demonstrated in multiple studies to be highly predictive of uid responsiveness in hypo-
tensive patients. One of the simplest dynamic challenges that is useful in a spontane-
ously breathing patient is to assess the change in cardiac index (CI) or stroke volume
Common clinical manifestations: index (SVI) caused by passive leg raising. A baseline measurement is obtained with the
Neurological: patient sitting 30 degrees upright. The patient is quickly lowered to the supine position
A. Anxiety, Delirium, Altered level of consciousness ranging from somnolent to and the legs are manually raised to 30 to 45 degrees. This causes a central redistribution
unresponsive of about 500 mls of blood in the average adult. An increase in CI or SVI of > 10% is a
B. Inability to protect airway powerful predictor that the patient will respond to a subsequent uid bolus.
A. Tachypnea There are a host of other dynamic parameters that can be employed in more critically
ill patients who are being supported with mechanical ventilation. Positive pressure
B. Hypoxemia mild hypoxemia with a clear CXR to severe ARDS ventilation increases intrathoracic pressure, which impairs right ventricular lling and
Cardiovascular: may cause over distension of the lung in some patients. This in turn could increase right
A. Hypotension (SBP < 90 mm Hg or more than 40 mm Hg less than baseline) ventricular afterload. These effects are greater in hypovolemic patients and result in a
B. Tachycardia fall in right ventricular stroke volume with inspiration. The reduced right ventricular
C. Extremities may be cool and mottled or warm with brisk capillary rell (after stroke volume leads to a reduced left ventricular stroke volume in the cardiac cycle.
volume resuscitation) depending upon the etiology of shock The variation in stroke volume is seen as changes in systolic blood pressure and pulse
pressure, pulse oximeter pulse variability index or stroke volume variation. All of these
can be used to predict whether a patient is likely to respond to the next uid bolus. 1. Adequate or normal oxygen delivery (DO2)
There are several conditions that need to be present to use dynamic parameters to a. DO2 = (1.34 X Hgb X SaO2) + (0.003 X PaO2)
predict uid responsiveness. The patient should not be over breathing the ventilator 2. Normal cardiac index (CI) and in many cases normal or optimal stroke volume
and should be receiving a tidal volume of 8 ml/kg predicted body weight. The patient index (SVI). Supranormal CI or DO2 has not been proven to be benecial once
is likely to respond to a subsequent uid bolus if signicant variation is present in the shock has ensued.
dynamic parameter ( Systolic Blood Pressure, Pulse Pressure, Pleth Variability 3. SCVO2 > 70%
Index, Stoke Volume Variation, Velocity Time Integral variation with esophageal Dop-
pler monitoring, etc.). The patient should be in a regular cardiac rhythm otherwise each 4. Clearance of lactic acidosis
stroke volume is different because of different R R intervals and diastolic lling time. B. Maintain an adequate blood pressure. MAP 65 mm Hg is the most commonly
Dynamic parameters may also not be useful in patients with an open thorax, abdominal recommended goal although there is likely signicant patient-to-patient variation for
compartment syndrome or severe right ventricular failure. an optimal target. Available monitoring technologies do not allow for identication
of patient specic optimal blood pressure targets.
During volume resuscitation it is imperative that close attention be paid to the patients C. Avoid hydrostatic pulmonary edema.
pulmonary status so that any subtle worsening such as decreased oxygenation or pul- D. Avoid myocardial injury.
monary detected before and even during each uid bolus. Pulmonary E. Avoid precipitating abdominal compartment syndrome by avoiding excessive
deterioration during volume resuscitation should lead the clinician to carefully reassess crystalloid resuscitation.
the patients condition before proceeding with successive volume administration.
Therapeutic Recommendations
The concept of oxygen transport has been attempted to be used for decades to help Airway and breathing:
guide resuscitation. Both the logic and the mathematics are very appealing but despite The rst consideration in any unstable patient is whether or not the patient is able to
numerous investigations there has been only one study in over 40 years, which has protect their airway and maintain appropriate levels of oxygenation and minute ventila-
demonstrated an improvement in outcome using this approach in patients with shock. tion. This assessment and decision is particularly crucial for the patient in shock. There
This study randomized patient with severe sepsis or septic shock in the Emergency is no role for noninvasive ventilation in a patient who is in shock. Patients in shock
Department to standard therapy or early goal directed therapy (EGDT), which targeted may not show a progressive rise in their PaCO2 as an indicator of respiratory deterio-
a central venous oxygen saturation (SCVO2) of > 70 % during the rst 6 hours of care. ration. Instead they may have ongoing vasopressor requirements and many times a
The patients who received EGDT had a lower mortality and fewer complications. worsening metabolic acidosis before they abruptly suffer a respiratory arrest with dire
This study forms the basis for the rst two recommendations of the Surviving Sepsis consequences.
Campaign. Unfortunately, this studys ndings have not yet been replicated although
there are several ongoing studies at the current time. To complicate matters, numerous
other studies have not found any cost or outcome benet with monitoring mixed venous Fluid therapy:
oxygen saturation (SVO2). There is also no consistent relationship between changes in There is now reasonable data to assist in making rational uid choices in shock resusci-
the SCVO2 or SVO2 and the cardiac index even in cardiac or cardiac surgery patients. tation. There is repeated observational data that in trauma patients, who require massive
However, a low and falling SVO2 (or SCVO2) in an unstable patient may be an ominous transfusions (2 -3 % of all civilian trauma cases), resuscitation with packed red blood
sign and an indication to measure the key components of oxygen delivery and reassess cells (PRBCs) and fresh frozen plasma in a 1:1 ratio may improve outcomes. There
oxygen demand. may also be benet to the 1:1:1 administration of platelets with PRBCS and FFP.

Echocardiography, both transesophageal and transthoracic, has become an essential tool The administration of 0.9% normal saline results in the same clinical outcomes as 4%
to help determine the etiology of shock and help guide therapy. One can rapidly deter- albumin in a wide range of critically ill patients. Hydroxyethyl starch (HES) prepara-
mine global left and right ventricular function, evaluate for the presence of pericardial tions of all kinds are associated with worse outcomes in patients with septic shock and
uid, and assess inferior vena cava size and collapsibility as an indicator of uid respon- the FDA has released a statement that HES solutions should not be given to critically ill
siveness. More advanced echocardiographers can assess for valvular function, evidence patients including those with sepsis, and those admitted to the ICU.
of outow tract obstruction, and superior vena cava collapsibility. Echocardiography
can be rapidly performed in every patient who is not responding well to resuscitation Fluids for resuscitation should be given as patient and disease appropriate boluses over
efforts and perhaps in most if not all patients in shock in an intensive care setting. Com- 5 10 minutes, looking for an effect on blood pressure, heart rate, cardiac output, perfu-
bining the ndings on one or more echocardiographic examinations with continuous sion and most specically the stroke volume index (SVI). The primary hemodynamic
assessment of cardiac index, stroke volume index or another dynamic predictor of uid purpose of administering a uid bolus is to increase preload to augment the SVI. If the
responsiveness is an excellent contemporary way to guide shock resuscitation. (Please SVI is low and not increasing with appropriate uid boluses, then the problem is likely
see chapter 9, Ultrasound in the ICU). not hypovolemia and an alternative diagnosis needs to be pursued. An echocardiogram
at this point may be helpful. Close attention should be given to the patients pulmonary
Goals of Resuscitation status during volume resuscitation.
A. Rapidly restore tissue perfusion by obtaining:
Vasoactive medications norepinephrine for severe hypotension (SBP < 70 mm Hg) although data from a
Vasopressors recent prospective trial suggests norepinephrine may be a superior agent.
There are now large well conducted randomized controlled trials to help guide the C. Consider mechanical support with IABP, which may not be benecial, or VAD.
choice of vasopressors in different shock states. Norepinephrine is superior to dopa- D. Urgent revascularization (thrombolytic, PCI or surgery) if ischemic heart disease
mine in multiple different categories of shock. The use of norepinephrine is associated is the cause.
with the rate of atrial brillation (11% vs. 22%) compared with dopamine in cardio- E. Fluid administration may not be helpful. Only a small percentage of patients will
genic, septic and hypovolemic shock. Several systematic reviews suggest that the use be hypovolemic because of excessive diuresis or other processes.
of dopamine may be associated with higher mortality in septic shock. Vasopressin use
is associated with signicant reductions in other vasopressor use in septic shock and in Cardiogenic shock - post-cardiac surgery:
patients with vasodilated shock following cardiac surgery.
A. Fluid resuscitation may be necessary because of vasodilation and ongoing losses.
B. Correct coagulopathy.
C. Optimize pacing.
Dobutamine, epinephrine and the phoshodiesterase inhibitors are inotropes used in dif-
ferent clinical situations based upon pharmacological activities and historical practice. D. Transesophageal echocardiography can be useful
There are no comparative outcome trials. Phosphodisterase inhibitors, such as milri- E. Dobutamine and epinephrine are commonly used as inotropic agents. Limited
none, cause pulmonary vasodilation and can be a good choice in a patient with pulmo- data suggests epinephrine may succeed when dobutamine has been ineffective.
nary hypertension or right heart failure. F. Phosphodiesterase inhibitors can be employed as inotropic agents and as a
pulmonary vasodilator. They will also cause signicant systemic vasodilation
Mechanical Cardiac Support which may have to be corrected with a vasopressor such as norepinephrine.
The combination of a beta adrenergic agonist, like epinephrine, with a
There are a variety of different options for supporting a patient in shock including intra- phosophodiesterase inhibitor is a potent inotropic combination.
aortic balloon pumps (IABP), ventricular assist devices (VAD) and veno-arterial extra-
corporeal membrane oxygenation (ECMO). (Please see chapter 23, ECLS and VAD) G. Norepinephrine may be used to treat signicant vasodilation if optimal
intravascular volume and inotropic support are ensured.
H. Vasopressin in physiological replacement doses (0.03 0.04 mcg/kg-min) may
Recommendations for selected shock states: allow signicant decreases in the dose and duration of administration of other
Hypovolemic: vasopressor agents.
A. Patient who is NOT bleeding I. Mechanical circulatory assistance, VAD or V-A ECMO, may be required. An IABP
1. Isotonic crystalloids is still employed in this setting at times but any increase in CO would be expected to
2. Albumin be modest at best.
3. No HES
B. Hemorrhagic shock Obstructive shock - Pulmonary embolism:
1. Obtain excellent intravenous access A. Acute right ventricular failure is usual cause of demise.
2. Avoid excessive use of crystalloids and albumin B. Ensure adequate systemic anticoagulation unless contraindicated.
3. Anticipate effects of next round of uids/ blood products (i.e. Patient with Hgb C. Add inotropic agent to support right ventricular function with consideration for
7.3 gm/ dl and giving 4 units of FFP; must also give PRBCs if pulmonary status phosphodiesterase inhibitor.
allows) D. Consider systemic thrombolytic therapy in appropriate candidates.
4. Check coagulation status (conventional tests and viscoelastic tests) and correct E. Consider surgical embolectomy if patient is not a candidate for thrombolytic
abnormalities aggressively therapy.
C. Severe trauma with hemorrhagic shock requiring massive transfusion F. Consider inhaled pulmonary vasodilators: inhaled prostacyclin PGI2 and nitric
1. PRBC:FFP ratio of 1:1 oxide.
2. Early administration of platelets may be helpful G. Consider V-A ECMO
3. Tranexamic acid (TA); if less than 3 hours after injury; 1 gram IV over 10
minutes followed by 1 gram IV over 8hr Obstructive Shock - Cardiac tamponade:
A. May have modest initial improvement with uid bolus.
Cardiogenic shock - Medical patient: B. Echocardiography for diagnosis
A. Echocardiography to assess for ventricular and valvular function and to look for C. Norepinephrine to support blood pressure
complications ventricular septal defect, ruptured chordae tendinae D. Urgent drainage of pericardial uid by pericardiocentesis, pericardial window or
B. Historical practice has been to use dopamine and dobutamine and reserve sternotomy depending upon the setting.
Vasodilated or distributive shock - Septic shock: Questions:
A. Volume resuscitation guided by dynamic parameters and clinical response.
18.1 Which statement regarding uid therapy is correct?
B. Isotonic crystalloid or albumin (HES products are contraindicated) A. Transfusion to Hgb > 12 gm/dl improves tissue oxygen delivery and outcomes in pa-
C. Norepinephrine is rst choice for vasopressor to maintain MAP 65 mm Hg. tients with shock.
B. Hydroxyethyl starch preparations are proven to be safe and effective agents in critically
D. 1/3 of adult patients with septic shock will have signicant myocardial ill patients at risk for renal failure.
depression. Echocardiography should be performed in many patients with septic C. The use of 4% albumin or 0.9% Normal Saline has been shown to result in similar clini-
shock. cal outcomes in a wide variety of critically ill patients.
D. Crystalloid resuscitation has been demonstrated to result in better outcomes than 4 %
E. Some patients will require inotropic support with dobutamine or epinephrine to albumin in patients with septic shock.
achieve a normal CI and SVI.
F. Hydrocortisone 200 mg/day may be considered in patients requiring more than 18.2 Which of the following predicts uid responsiveness in a critically ill patient?
one vasopressor. This can be given in divided doses (50mg q6h) or as an infusion of A. Stroke volume variation
9mg/h. B. Central venous pressure
C. Cardiac output
G. Aggressive resuscitation must be combined with successful treatment of the D. Pulmonary artery wedge pressure
infectious or inammatory cause of septic shock.
18.3 Which of the following statements are true regarding the use of vasopressors in shock?
A. Dopamine use causes a much higher rate of atrial brillation than norepinephrine in
Summary patients with shock.
The care of the patient with shock is challenging and requires aggressive efforts to B. Norepinephrine may be associated with a higher survival rate than dopamine in patients
restore and maintain tissue perfusion while avoiding harm. Newer approaches such as with septic shock.
C. The addition of vasopressin to norepinephrine has not been shown to improve clinical
the use of dynamic parameters to predict uid responsiveness and bedside echocardiog- outcomes in patients with septic shock.
raphy performed by Intensivists has radically changed the approach to monitoring and D. All of the above
guiding therapy.

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9. Dellinger RP, Levy MM, Rhodes A et al: Surviving sepsis campaign: international
guidelines for management of severe sepsis and septic shock

19. Diagnosis and Treatment of Dysrhythmias
Ryan Laterza MD and Adam S Evans MD

Key Points A 71 year-old woman with a history of COPD, HTN, and DM type 2 has
been in the ICU for 2 days following a 3 vessel CABG. The nurse calls you
Dysrhythmias are common in the intensive
because the patient has a marginal BP, low urine output, and this ECG
(gure 19.1) for 2 hours, and now she seems more lethargic
care unit

When evaluating a patient with a

dysrhythmia, first determine if the patient
is hemodynamically stable, then obtain a
12 lead ECG to answer: Is the rhythm slow or
fast? Regular or irregular? Are QRS complexes
narrow or wide (>120 ms)? Does every P have
a QRS?
Figure 19.1 Rhythm Strip
Ventricular fibrillation (VF) is incompatible
with life. Only immediate defibrillation will
convert VF into a life-sustaining rhythm.
Dysrhythmias are common in the intensive care unit (ICU) and complicate the management of patients with
sepsis, renal failure, pulmonary disease, coronary ischemia and heart failure. Surgery is a major risk factor
in the development of post-operative dysrhythmias due to pain, inammation, electrolyte abnormalities, and

This chapter is not meant to serve as an exhaustive description of the morphology, pathophysiology, and treat-
ment of all known and unknown arrhythmias! It is intended to help house staff quickly review and understand
the current treatment options in managing the most common arrhythmias encountered in the ICU.

Atrial Bradyarrhythmias
1. Sinus Bradycardia (SB) is often caused by decreased automaticity within the sinoatrial (SA) node. This
can be secondary to increased vagal tone, absent sympathetic tone (e.g., high spinal), hypothyroidism,
intracranial hypertension, hypothermia, drug toxicity, electrolytes, coronary ischemia, or primary SA node

2. Sinoatrial disease or sick sinus syndrome (SSS) is a degenerative disease of the conduction system
including the SA and atrioventricular (AV) nodes. It is characterized by symptomatic bradycardia, frequent
sinus pauses, sinus arrest, junctional escape rhythms, and sinus bradycardia with 4. Premature atrial contractions (PACs) arise from areas of ectopic foci in the atria.
paroxysmal atrial brillation. Most patients are asymptomatic with palpitations being the most common complaint.
PACs are often caused by excessive caffeine, ethanol, stress or hyperthyroidism. They
3. AV nodal blockade (AVB) may be incomplete (1st and 2nd degree) or complete are differentiated from a PVC by their narrow QRS complex, presence of a P wave,
(3rd degree). The block may be temporary or permanent, and is caused by a variety of and a short compensatory pause.
drugs and diseases. Common pharmacologic offenders are adenosine, calcium channel
blockers, beta blockers, amiodarone, and digoxin. Inammatory and inltrative 5. Atrial utter is characterized by an atrial rate that is generally 300 +/- 20 bpm, with
disorders (e.g., sarcoidosis), coronary ischemia, myocarditis, thyroid disorders, and variable conduction through the AV node (usually 2:1). The typical sawtooth pattern
malignancy can also lead to AVB. This rhythm is also a known complication following is most prominent in lead II on ECG.
aortic or mitral valve surgery.
6. Atrial brillation is characterized by an irregularly irregular rhythm. The atrial rate
4. First degree AVB is dened as a PR interval > 200 ms. It is caused by a slow is often around 300-400 bpm with variable conduction and loss of AV synchrony. The
conduction through the AV node and rarely requires intervention. Second degree AVB ventricular rate is usually 100-180 but can be higher in the presence of an accessory
usually reects disease at the AV node (Mobitz I) or the His- Purkinje system (Mobitz tract. High ventricular rates, known as rapid ventricular response (RVR), can lead to
II). Mobitz Type I (Wenckebach) is an irregular pattern of progressive PR interval fatigue, heart failure, angina, and cardiovascular collapse.
lengthening until a QRS complex is dropped. It is usually transient and typically does
not need treatment. Mobitz Type II is an irregular pattern of complete conduction
blockade, resulting in randomly dropped QRS complexes without changes in the PR
interval. The ventricular rate depends on the frequency of dropped beats. This type of Ventricular Dysrhythmias
AVB can proceed to complete third degree heart block. Third degree AVB is complete 1. Ventricular dysrhythmias are characterized by the absence of an associated P wave
atrioventricular dissociation caused by atrial impulses not conducting through the and often have a wide QRS complex (> 120 ms). Ventricular bradyarrhythmias are
AV node. The ECG will show independent atrial and ventricular rates with an escape commonly ventricular escape rhythms caused by pacemaker sites distal to the AV
rhythm from an ectopic focus distal to the block. The escape rhythm can have a node (e.g., 3rd degree AVB).
narrow or wide QRS complex, with a HR of 40-60 bpm.
2. Premature ventricular contractions (PVCs) arise from one or more ectopic foci
5. Pulseless electrical activity (PEA) is organized electrical cardiac activity without distal to the AV node. They are distinguished by their wide QRS complex, lack
mechanical activity. Asystole refers to the complete absence of electrical and of a P wave, and long compensatory pause. The premature contraction leads to a
mechanical activity of the heart. decrease in stroke volume which is balanced by an increase in stroke volume after
the compensatory pause on the following beat. PVCs may occur in normal hearts,
but increasing PVC frequency may indicate coronary ischemia, valvular disease,
Atrial Tachydysrhythmias cardiomyopathy, electrolyte disturbance, or a prolonged QT interval. They may also
1. Any rapid heart rate (> 100 bpm) that originates from the atria is referred to as a occur as a result of direct irritation from central catheters and guidewires.
supraventricular tachycardia (SVT). They are categorized by their rhythm (regular vs.
irregularly irregular) and generally have a narrow QRS complex.
3. Ventricular tachycardia (VT) can be dened by morphology (monomorphic vs.
polymorphic), duration (sustained vs. non-sustained), and physical exam ndings
2. Sinus tachycardia (ST) is dened as a heart rate > 100 bpm with 1:1 AV (pulse vs. pulseless). VT is generally caused by conditions which predispose the
conduction and a regular rhythm. It can be differentiated by other types of SVT by myocardium to reentry or make it more susceptible to develop abnormal automaticity
its gradual onset and resolution. Common causes include pain, alcohol withdrawal, such as ischemia, long QT interval, and heart failure.
hyperthyroidism, and pulmonary embolism.
a. Monomorphic VT is characterized as a wide complex, xed morphology, regular
3. Reentry SVT can be caused by AV nodal reentry tachycardia (AVNRT) and AV rhythm tachycardia. It can be well tolerated by some patients, but often is associated
reentry tachycardia (AVRT). Reentry SVT is characterized by a self-perpetuating with symptoms of cardiac failure such as dyspnea, syncope, hypotension, and oliguria.
reentry circuit between the atria and ventricle. The rhythm is regular and the b. Polymorphic VT has an irregular QRS pattern and is often an irregular rhythm. It
morphology often shows a narrow QRS complex. Wolff-Parkinson-White (WPW) is can quickly deteriorate into ventricular brillation.
the most common form of AVNRT and involves an AV bypass tract (i.e., bundle of
Kent). WPW patients often complain of paroxysmal symptoms of palpitations and
dyspnea. Their ECG ndings show a decreased PR interval and the characteristic 5. Torsades de Pointes (TdP) is a polymorphic VT associated with a long QT interval.
delta sign caused by early ventricular depolarization leading to a widen QRS. AV It appears as a sine wave rotating on its own axis. It typically occurs when the QTc
nodal blocking agents should be avoided in WPW patients with atrial brillation interval has been excessively prolonged (> 500 ms) and is often iatrogenic from
because they can paradoxically increase their HR. antiarrhythmic agents (e.g., sotalol, procainamide), antipsychotic medications (e.g.,
haloperidol and droperidol), and methadone.

hypotension, and AVB.
6. Ventricular brillation (VF) is incompatible with life. There is no associated
pulse as the ventricle does not contract in an organized manner. It is associated with 3. Beta-blockers also have negative chronotropic and inotropic effects on the heart.
ischemic cardiac disease and is thought to be caused by reentry circuits and abnormal This class of medication is contraindicated in patients with decompensated heart
automaticity. Only immediate debrillation will convert VF into a life-sustaining failure and high-degree AVB.
4. Amiodarone (150 mg IV bolus over 10 minutes followed by infusion) acts on Na+,
K+, and Ca++ channels, as well as alpha and beta receptors. This causes prolongation
MANAGEMENT of the myocardial action potential and refractory period, as well as decreasing the
When evaluating a patient with a dysrhythmia, obtain a 12 lead ECG, and answer the effect of circulating stress hormones (decreasing intracellular calcium). Amiodarone
questions below. Knowing the answers to these questions will help guide pharmacologic is effective in controlling the rate of all SVTs, including atrial brillation, and is
and electrophysiologic treatment, and suggest underlying causes to treat. indicated for refractory/recurrent VT and VF as well. Amiodarone has a very long
half-life (approximately 60 days), and patients must be loaded to reach meaningful
levels quickly. The amiodarone load can cause hypotension, bradycardia, and
1. Is the rhythm slow or fast? sinus arrest acutely. Long term side effects include pulmonary toxicity, ventricular
2. Is it regular or irregular? dysrhythmias, rare hepatic toxicity, CNS symptoms, and thyroid dysfunction.
3. Are the QRS complexes narrow or wide (>120 ms)?
4. Does every P have a QRS and does every QRS have a P? 5. Digoxin inhibits the Na+/K+-ATPase membrane pump and through this
5. Is the patient hemodynamically stable? mechanism indirectly increases the intracellular calcium concentration. It is a positive
inotrope and prolongs the refractory period of action potentials reducing the maximum
Bradycardia frequency of conduction through the AV node. It has a delayed peak effect (up to 6
hours), and a narrow therapeutic index (especially in the setting of hypokalemia).
Treatment for bradycardia should be reserved for symptomatic patients and is often well
tolerated until the HR is < 40 bpm. The mainstay of therapy is treating the underlying
cause or removing the offending agent.
Other Treatment Modalities
1. Atropine (0.5 mg IV per dose, every 3 to 5 min) is a vagolytic that can be used
to temporarily treat bradycardia until denitive treatment is available. Atropine is 1. For SVT and ventricular dysrhythmias alternative options include lidocaine,
ineffective after cardiac transplant and in symptomatic bradycardia secondary to procainamide, sotalol, ecainide, and dipyridamole. Optimizing the patients
Mobitz Type II and Third degree AVB. electrolytes by maintaining the magnesium greater than 2 mg/dL and the potassium
greater than 4 mEq/L is also helpful in preventing reoccurrence of the arrhythmia.
2. Epinephrine (2-10 mcg/min IV) is a potent 1 agonist which increases HR and
contractility, as well as systemic vascular resistance (via 1 receptor activity). 2. Synchronized cardioversion refers to the delivery of an electrical current to the
Epinephrine administration can lead to tachydysrhythmias. Electrical pacing via a myocardium synchronized to the R wave. This allows the delivered shock to safely
transcutaneous or transvenous route is recommended in cases of Mobitz II and 3rd depolarize all excitable tissue simultaneously, resetting all myocardial tissue to the
degree AVB. same refractory period. This is thought to allow the dominant pacemaker cells to
resume function and thereby suppress areas of ectopy and reentry. Complications of
Tachycardia cardioversion include embolic events (particularly in atrial brillation), skin burns,
myocardial dysfunction, dysrhythmias, and transient hypotension from myocardial
Treatment of tachydysrhythmias should be focused on correcting underlying causes. stunning.
Treatment is aimed at suppressing automaticity, prolonging the effective refractory time,
and facilitating normal impulse conduction.
3. Debrillation refers to the non-synchronized delivery of massive amounts of
energy with the intent of depolarizing all of the myocardium simultaneously. If the
1. Adenosine (1st dose: 6 mg and 2nd dose: 12 mg rapid IV bolus) blocks the AV energy is insufcient to completely affect all cardiac tissue, areas of brillation
node, slows conduction time, and blocks reentry circuits. It is indicated for patients will remain and the heart will revert back after the refractory period. In addition, it
with a reentry SVT. Side effects are coronary vasodilatation, bronchoconstriction, and seems that with time, ventricular brillation is more difcult to convert. Therefore,
ushing. in pulseless VT/VF, it is recommended that high energy shocks (360J monophasic or
150-200J biphasic) be delivered as soon as possible.
2. Calcium channel blockers (CCB) have negative chronotropic (reduce SA ring)
and dromotropic (slow conduction through the SA node) properties. This allows
them to be very effective at rate control for most SVTs. Side effects are bradycardia,
This chapter is a revision of the chapter authored by Isaac Lynch, MD and Michael H. Wall, MD
19.1 The ICU resident is called by a nurse to evaluate a 22 year-old man complaining of palpita-
tions and dyspnea. He is post-operative day two from an appendectomy. His HR is 155 and his
1. Breitkreutz R. WF, Seeger F: Focused echocardiographic evaluation in resuscitation BP is 88/58. His ECG shows an irregularly irregular wide complex rhythm. The intern gives meto-
management: Concept of an advanced life support-conformed algorithm. Crit Care Med prolol 5 mg IV push and the patients mental status deteriorates. Vitals are now HR 205 and BP
2007;35(5 Suppl):S150-61 71/37. Which of the following in this patients history is most consistent with the condition that
2. Dobrev D, Nattel S: New antiarrhythmic drugs for treatment of atrial brillation. Lan- resulted in this paradoxical response?
cet 2010;375:1212-23
3. Kleinman ME, Chameides L, Schexnayder SM, Samson RA, Hazinski MF, Atkins DL,
Berg MD, de Caen AR, Fink EL, Freid EB, Hickey RW, Marino BS, Nadkarni VM, Proctor A. History of chest pain exacerbated by exertion alleviated by rest.
LT, Qureshi FA, Sartorelli K, Topjian A, van der Jagt EW, Zaritsky AL: Part 14: Pediatric B. History of dyspnea when lying at.
Advanced Life Support: 2010 American Heart Association Guidelines for Cardiopulmo- C. History of paroxysmal palpitations, shortness of breath, and dizziness.
nary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122 (18 suppl D. History of sharp chest pain radiating towards the back.
4. Lafuente-Lafuente C, Mahe I, Extramiana F: Management of atrial brillation. BMJ 19.2 A 61 year-old man is post-operative day number two following a mitral valve repair. His
2009;339:b5216 ECG shows an irregularly irregular narrow complex tachycardia with a HR of 145. His vitals are
5. Menke J, Lthje L, Kastrup A, Larsen J: Thromboembolism in Atrial Fibrillation. Am J HR 151, BP 120/52, SpO2 96% on room air. His preoperative TTE showed an LVEF of 55%.
Cardiol 2010;105(4):502-10 Which of the following is the most appropriate initial therapy?
6. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk
PJ, Ornato JP, McNally B, Silvers SM, Passman RS, White RD, Hess EP, Tang W, Davis D,
Sinz E, Morrison LJ: Part 8: Adult Advanced Cardiovascular Life Support: 2010 American A. Amiodarone
Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardio- B. Metoprolol
vascular Care. Circulation 2010;122(18 Suppl 3):S729-67 C. Digoxin
7. Schirmer SH, Baumhkel M, Neuberger H-R, Hohnloser SH, van Gelder IC, Lip GYH, D. Cardioversion
Bohm, M: Novel Anticoagulants for Stroke Prevention in Atrial Fibrillation: Current Clini-
cal Evidence and Future Developments. J Am Coll Cardiol 2010:56(25):2067-76 19.3 A 74 year-old woman is status post a three-vessel CABG. On post-operative day one, she
is found to have an altered mental status and is having difculty breathing while lying at. Her
vitals are HR 32 and BP 72/32. ECG shows what appears to be complete disassociation between
the P wave and the QRS complex. Which of the following would be the best initial step in man-

A. Atropine
B. Chest Compressions
C. Cardioversion
D. Cardiac Pacing

20. Diagnosis and Treatment of Myocardial Ischemia
Katie Menzel MD and Dawn Nye DO

Key Points A 70-year-old male is admitted to the ICU immediately post-operatively

following a radical cystoprostatectomy with ileal conduit creation. Blood
The risk of PMI peaks within the first three
loss was 2L and 4 units PRBC were transfused. He arrives intubated
with stable vital signs. His past medical history includes obesity,
postoperative days. hyperlipidemia, diabetes mellitus, and a 50 pack-year smoking history. On
postoperative day 0, he develops new hypotension and EKG changes.
Arrhythmias, acute heart failure, acute mitral
regurgitation are all acute complications of

Therapy is aimed at improving oxygen supply

versus demand ratio and various forms of

Anesthesiologists routinely care for and manage critically ill post-operative patients, whose unique character-
istics increase their risk of myocardial ischemia and infarction. Early recognition and therapeutic intervention
of acute myocardial ischemia is critical to reducing morbidity and mortality.

Myocardial ischemia or infarction can occur any time myocardial oxygen demand exceeds supply. In the post-
operative patient, this can be due to either the disruption of an atheromatous plaque resulting in intracoronary
thrombus or to an imbalance between the supply and demand of oxygen from other causes. The latter mecha-
nism is likely the most common scenario leading to post-operative MI (PMI) in the ICU and is sometimes
called demand ischemia.

Myocardial oxygen supply

The myocardium is perfused by the coronary arteries, which arise from the aortic root (Figure 20.1). The
difference between aortic and ventricular pressures determines the coronary perfusion pressure. In the left
ventricle, due to high systolic, transmural pressures, perfusion of the subendocardium occurs exclusively dur-
ing diastole. Because of its lower ventricular pressure, the right ventricle is perfused throughout the cardiac
cycle. If the aortic diastolic pressure is low, or if the ventricular end-diastolic pressure is sufciently high to
impede forward ow, myocardial ischemia may occur. Additionally, as the heart rate
increases, less time is spent in diastole, thereby decreasing coronary perfusion.

Smaller arteries have increased resistance to ow as governed by Poiseuilles law; as

their radius decreases, ow decreases exponentially. Thus, even without plaque rupture,
patients with atheromatous or small coronary arteries are at increased risk for MI.

Finally, blood that reaches the myocardium must be adequately oxygenated in order
to fuel metabolism and prevent ischemia. Increased hemoglobin and oxygen satura-
tion (and to a lesser extent PaO2) will all increase the oxygen content of blood. Oxygen
content = 1.36*SaO2*Hgb + 0.003*PaO2

Myocardial oxygen demand

As the number or force of cardiac myocyte contractions increase, the oxygen demand
increases. Therefore, oxygen demand is proportional to heart rate, wall tension, and

Postoperative Myocardial Infarction (PMI) Mechanisms

The risk of PMI peaks within the rst three postoperative days. Several physiologic
changes contribute to this risk:
Extravascular uid mobilization increases preload and myocardial wall stress
Prothrombotic state from coagulation cascade activation and inammation
Catecholamine surges (including related to post-operative pain) increase heart rate
and blood pressure
Figure 20.1 The surface anatomy of the heart, viewed anteriorly.
In addition to altering the balance of myocardial oxygen supply and demand directly,
these changes predispose individuals with atherosclerosis to plaque rupture. specic coronary artery. Other nonspecic ST or T wave changes can also occur in MI.

Diagnosis Injured myocardial cells release enzymes that can be measured as biomarkers of MI.
While cardiac troponins T and I are currently the most sensitive and specic biomark-
The signs of PMI may be as nonspecic as altered mental status, arrhythmia, or shock. ers, they may also be elevated in heart failure and renal insufciency and are not suf-
Chest pain may be masked by analgesics, and intubated patients often cannot communi- cient to rule in MI.
cate symptoms. Furthermore, symptoms can often be attributed to many other causes in
a post-operative patient.
Echocardiography can also be useful in the assessment of regional wall motion, valve
function and overall cardiac function. Regional wall motion abnormalities are espe-
Electrocardiography (ECG) may show a number of changes. Elevation or depression cially helpful if there is a prior study available for comparison. Echocardiography also
of the ST segments in a regional distribution of leads suggests ischemia arising from a allows noninvasive measurements of some hemodynamic parameters, including right
and left sided pressures and cardiac output.

Table 20.1 Differential diagnosis based on common EKG changes, Echo Once a diagnosis of myocardial ischemia is made, cardiac catheterization and angiogra-
changes and symptoms phy is used to identify the anatomic location of the culprit atherosclerotic lesion (Figure
Tako-tsubo Pericarditis Pulmonary Pneumothorax Hypovolemia 20.2).
cardiomyopathy Embolus
EKG changes + + +*
Echo changes + +*
Symptoms + + + + +
*may see pattern of right heart strain on EKG and/or right heart failure on echo
Classication Type 3: sudden unexpected cardiac death
Several classication schemes exist to describe MI: Type 4a: associated with percutaneous coronary intervention (PCI)
Type 4b: in stent stenosis
Anatomic: Type 5: associated with CABG
Transmural versus nontransmural
Involved segments of myocardium (inferior, anterior, septal, etc.) Complications:
There are several serious complications of MI to be aware of when treating critically ill
EKG: post-operative patients.
Q wave MI versus non Q wave MI
ST elevation MI (STEMI) versus non-ST elevation MI (NSTEMI) Electrical
Bradyarrhythmias: occur when the conduction system becomes ischemic.
Clinical: Based on 3rd universal denition of MI from the 3rd Global MI Task Force Sinus bradycardia, junctional bradycardia with or without ventricular escape, and
Type 1: due to a primary coronary event (plaque rupture, dissection) complete heart block.
Type 2: due to imbalance in supply and demand

Figure 20.2 Cardiac Catheterization: The image on the left demonstrates stenosis of the left main artery (LMA). The image on the right demonstrates stenosis of the
right coronary artery (RCA)

Tachyarrhythmias: occur when ischemia leads to irritability of the myocardium and
disorganized transmission of electrical impulses.
Atrial: sinus tachycardia, supraventricular tachycardias (SVTs) and atrial brillation
or utter with or without rapid ventricular response
Ventricular: ventricular tachycardia (VT) and ventricular brillation (VF)

Acute heart failure: occurs when impaired myocardial function reduces cardiac output.
Left heart failure symptoms include: pulmonary edema, pulmonary hypertension,
and cardiogenic shock.
Right heart failure symptoms include: peripheral edema, increased JVD,
hepatomegaly, and cardiogenic shock.

Wall rupture: occurs when infarcted tissue weakens and tears.

Usually occurs 2-7 days after completed infarct.
Can occur in the septum (ASD or VSD) or as free wall rupture.
Classic presentation is of cardiogenic shock and a new murmur.

Acute mitral regurgitation: may occur when rupture of ischemic papillary muscle causes
ail leaet and acute, severe MR.
Has a poor prognosis.
Usually occurs with inferior infarcts.
Classic presentation is of shock, pulmonary edema and a new murmur.

LV aneurysm: is caused by dyskinetic, scarred apical tissue leading to ballooning.

LV thrombus may form due to stasis and turbulent ow in LV aneurysm.
Embolisms may occur to organs supplied by the LV, including brain, kidneys,
extremities, and gut.
Persistent ST elevations are common in the apical territories, despite lack of active

Pharmacologic therapies
Antiplatelet agents: prevent platelet aggregation, adhesion and cohesion.
Aspirin (cyclooxygenase inhibitor) reduces mortality and is used as immediate
Thienopyridines (clopidogrel, ticlopidine) maintain stent patency after PCI.
Oxygen: improves PaO2, SaO2 and remains standard of care despite lack of evidence
for reduced morbidity or mortality.
Nitrates: dilate coronaries, improving subendocardial perfusion. Systemic
vasodilation reduces preload and afterload.
Effective in rst 48hrs of Ml
Avoid in acute inferior wall MI as it can cause profound hypotension.
Figure 20.3 Algorithm for diagnosis and management of postoperative MI in the ICU
Beta-blockers: decrease myocardial oxygen demand (decreased heart rate and
contractility), increase myocardial oxygen supply (increased diastolic time), and
reduce mortality in the rst week post-MI. They are also anti-arrhythmogenic.
Unfractionated heparin: inhibits thrombus propagation by activating anti-thrombin Left ventricular (LVAD), right ventricular (RVAD) or biventricular (BIVAD) assist
III. devices may be implanted to support cardiac output of a severely impaired ventricle.
Administered as infusion acutely until long-term anticoagulation is established Cannulation may occur emergently at the bedside or in the operating room.
G2b3a inhibitors (abciximab, eptibatide, tiroban): antagonize platelet G2b3a- The device is temporary but may be replaced with a permanent device as
receptors, inhibiting brin binding to platelets and platelet aggregation. destination therapy or a bridge to transplant.
Use during PCI reduces mortality, reinfarction, and need for further
revascularization. Extracorporeal membrane oxygenation (ECMO):
ACE inhibitors: reduce afterload through vasodilation and are recommended within Blood is circulated and oxygenated through an external heart-lung machine.
24 hours of AMI as tolerated by blood pressure. High risk for complications including bleeding, infection, ischemia, compartment
Use caution in patients with renal injury. syndrome.
Statins: reduce inammation, improve endothelial function, reverse prothrombotic Temporary
states, and reduce atherosclerotic plaque volume.
High intensity statin therapy (atorvastatin 80mg) reduces early recurrent ischemic Intra-aortic balloon pump
events compared to moderate therapy (40mg) or placebo.
provides intra-aortic counterpulsation.
Fibrinolytics (tPA): early use restores coronary blood ow in 50 80% of cases of
STEMI or new bundle branch block; however, signicant bleeding risk often prevents Inates during diastole, increasing myocardial perfusion
their use in the post-operative population. Deates during systole, creating negative aortic pressure and drawing blood
Hemodynamic support:
Contraindicated in patients with aortic regurgitation.
Inotropes (milrinone, dobutamine, epinephrine): increase myocardial contractility if
cardiac output is inadequate.
Vasopressors (norepinephrine, phenylephrine, vasopressin): increase peripheral
vascular resistance to increase mean arterial pressure.
Vasodilators (nitroglycerin, nitroprusside, nicardipine): reduce afterload to allow References
forward ow. 1. Practice alert for the perioperative management of patients with coronary artery
stents: a report by the American Society of Anesthesiologists Committee on Standards
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Invasive therapies myocardial infarction in noncardiac surgical patients. Chest 2006; 130:584-96.
Percutaneous coronary intervention: restores coronary ow in 90 95% of Ml patients 3. Fleisher, L. A., Beckman, J. A., Brown, K. A., Calkins, H., Chaikof, E., Fleischmann,
with a door to balloon time of less than 90 minutes. K. E., ... & Yancy, C. W.: ACC/AHA 2007 Guidelines on Perioperative Cardiovascular
Evaluation and Care for Noncardiac Surgery: Executive Summary A Report of the Ameri-
Preferable to brinolysis for PMI after noncardiac surgery given lower bleeding can College of Cardiology/American Heart Association Task Force on Practice Guidelines
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4. Kopecky SL: Effect of beta blockers, particularly carvedilol, on reducing the risk of
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5. Serruys PW, Morice MC, Kappetein AP, et al. Percutaneous coronary intervention
Must have appropriate anatomy versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med
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6. Thygesen K, Alpert JS, White HD: Joint ESC/ACCF/AHA/WHF Task Force for the
Urgent if patient is unstable due to anatomical complications of Ml Redenition of Myocardial Infarction: Universal denition of myocardial infarction. Eur
Heart J. 2007; 28:2525-2538.
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Transvenous pacemaker: Emergency transvenous leads may be placed to facilitate

temporary external pacemaking for unstable bradyarrhythmia. A permanent pacemaker
may be indicated if bradyarrhythmia does not resolve.

20.1 Which of the following pharmacologic therapies is not indicated for the acute treatment of
myocardial ischemia?
A. Nonselective cyclooxygenase inhibitor
B. Selective cyclooxygenase inhibitor
C. Angiotensin converting enzyme inhibitor
D. HMG-CoA reductase inhibitor

20.2 Which of the following will most improve the balance of myocardial oxygen supply and
A. Decrease in diastolic time
B. Decrease in heart rate
C. Increase in left ventricular end diastolic pressure
D. Increase in partial pressure of dissolved oxygen in blood

20.3 How does the treatment of myocardial infarction differ in post-operative patients as com-
pared to the general population?
A. Post-operative patients are at higher risk for infection from indwelling devices such as
transvenous pacemakers or ventricular assist devices
B. Post-operative patients are not candidates for coronary artery bypass grafting
C. Inotropes have been shown to impair anastomotic healing and should not be adminis-
tered to post-operative patients
D. Many pharmacologic therapies may be contraindicated due to an increased risk of surgi-
cal bleeding

21. Valvular Heart Disease
Sean Kiley MD

Key Points A 70 year old female, with no previous past medical history, presents
to the ER with an acute abdomen. Preoperative physical examination
Valvular heart disease may occur as a result
demonstrated a 4/6 systolic ejection murmur, but the emergent nature
of the case dictated immediate operative intervention without cardiac
of several processes including: infective work up. Intraoperatively, a 30 cm segment of small bowel was removed
endocarditis, inflammatory diseases, due to ischemia. The patient was extubated in the operating room but
congenital diseases, acute ischemia and experienced some shortness of breath in the PACU, initiating a transfer to
chronic degeneration. the ICU. Upon admission to the ICU the patients heart rate was 110 with
ST segment depression in the anterior and lateral leads. Transthoracic
Physiologic goals for aortic stenosis (AS) echo demonstrated aortic valve gradient of 55 mmHg and valve surface
are to keep HR low and the ventricle full with area of 0.7 cm2 in addition to a severely hypertrophied left ventricle, which
adequate diastolic pressure to avoid ischemia. demonstrated difculty lling. Fluid resuscitation was initiated along with
alpha 1-agonist therapy.
Physiologic goals for aortic regurgitation (AR)
are to maximize forward flow with afterload
reduction and increased heart rate. Intra-
aortic balloon pump (IABP) is contraindicated.
Mitral stenosis (MS) leads to left atrial Valvular heart disease can affect patients of all ages. It is most common in elderly patients, and, because the
enlargement and subsequent atrial fibrillation elderly population in the US is rising, it is likely that the incidence of valvular heart disease will rise as well.
with increased PA pressures. The most common valvular lesion is degenerative aortic stenosis followed by mitral regurgitation.

Mitral regurgitation (MR) also results in an Most valvular disorders are progressive without medical management. Even with the benet of medical man-
agement, many times these disorders require surgery for ultimate alleviation of symptoms. Recent progres-
enlarged left atrium with increased pulmonary sion in surgical technique has allowed many, who were previously considered inoperable, the opportunity for
artery (PA) pressures, which is treated with surgical repair.
afterload reduction. Unlike AR, IABP may be
useful in cases of acute decompensation. Each valvular disorder presents unique management challenges, and it is common for multiple disorders to
coexist, making management even more challenging. Patients with an existing valvular heart lesion who
present with an acute insult (systemic inammatory response syndrome (SIRS), sepsis, hemorrhage, etc.)
are at high risk for acute cardiovascular collapse, depending upon the severity of the lesion. The following
discussion aims at providing basic understanding of the causes of valvular heart disorders that are frequently
encountered in critically ill patients, as well as diagnostic and therapeutic interventions.
Aortic Stenosis (AS) moderate increase in contractility via beta-1 activity as well as preservation of
A. Pathophysiology systemic vascular resistance via alpha-1 activity. Patients receiving mechanical
ventilation need careful titration of sedatives and analgesic agents since these
1. In the elderly, degenerative calcication causes thickening and or fusion of agents can cause arterial hypotension. It is mandatory to treat pain rst and then
the valve leaets, which then inhibits opening surface area. This can also be a reassess patient for requirement of hypnotics to facilitate mechanical ventilator
congenital condition in which the patient is born with a bicuspid valve and the support and comfort.
stenosis progresses as the person ages.
D. Treatment
2. Persistent contraction against a xed resistance stimulates hypertrophy of the left
ventricular wall. This results in a stiffened left ventricle and diastolic dysfunction. 1. The medical goal is to maintain cardiac output while preventing volume
overload and pulmonary edema. This serves as a bridge to surgical or percutaneous
3. Severe stenosis reduces cardiac output. Severe left ventricular hypertrophy intervention.
(LVH) puts a high demand on diastolic perfusion pressure of the left ventricle.
This combination can cause acute ischemia. 2. There are several surgical procedures that may be utilized for corrective
therapy, depending on the patient and severity of the lesion. Percutaneous balloon
4. Severe stenosis causes progression to congestive heart failure. When this occurs, valvuloplasty, used for palliation, can cause severe aortic insufciency (AI).
the aortic valve pressure gradient is not reective of the severity of AS due to the Transcatheter aortic valve implantation for critical aortic stenosis is currently
low cardiac output. being used in patients not deemed surgical candidates; however, successes in this
B. Diagnosis procedure may lead to a broader application. Despite this, traditional open-heart
1. Symptoms include: angina, exertional dyspnea, syncope. surgery is still used for most cases.
2. Physical exam ndings include: soft ejection murmur, diminished aortic
component of S2, pulsus parvus et tardus, and brachio-radial delay. Aortic Regurgitation (AR)
3. ECG ndings include: LV hypertrophy, strain pattern T wave inversion and ST A. Pathophysiology
depression. 1. Regurgitant ow across the aortic valve can be caused by a number of different
4. Doppler echocardiography can be used to assess the severity by measuring processes including: abnormalities of aortic valve leaets (calcic degeneration,
maximum jet velocity and mean transvalvular gradient, which allows calculation bicuspid valves, destruction from endocarditis), aortic root dilation (aneurysm of
of aortic valve area. Direct measurement by planimetry can also be used to assess ascending aorta, aortic dissection), and endocarditis.
degree of stenosis. 2. Acute AR (acute dissection or acute endocarditis) can result in acute
5. Left heart catheterization can be used to calculate transvalvular gradient and cardiovascular decompensation.
valve area. 3. Chronic AR results in chronic pressure and volume overload, and causes
C. Management progressive ventricular dilation.
1. Invasive monitoring is often required for tight management of blood pressure B. Diagnosis
and uids. An arterial line should be utilized for second-to-second blood pressure 1. Physical ndings include a diastolic murmur, narrow pulse pressure, and
measurements. A central venous line (CVL) may be utilized for infusion of marfanoid features.
vasoactive drugs in acutely ill patients. Bedside ultrasonography is often helpful
for evaluation of uid status. 2. Echocardiography provides a denitive diagnosis. It may demonstrate thickened
valve leaets, ail leaets, a prolapsed valve, vegetations, and/or aortic root
2. Perioperative hemodynamic goals for patients with AS: dilation. A regurgitant jet will be apparent across the aortic valve on color ow
a. Maintain sinus rhythm and avoid tachycardia (60-70 beats per minute). Doppler. Transesophageal echo is useful for suspected thoracic aortic dissection.
Patients with concomitant aortic regurgitation may tolerate higher heart rates C. Management
(80 -90 beats per minute). Atrial contraction maximizes left ventricle preload.
Thus immediate cardioversion should be used in the setting of supraventricular 1. Perioperative goals are to decrease the regurgitant volume and maximize
arrhythmias causing hemodynamic instability. Appropriate post-operative forward systemic ow. Thus, relatively fast heart rate (90-100 beats per minute)
analgesia is important to prevent tachycardia. is preferred to decrease the time in diastole and subsequent regurgitant volume.
After load reduction may also be utilized.
b. Avoid hypovolemia. It is difcult to assess an appropriate volume status with
pulmonary artery catheter because the wedge pressure underestimates preload 2. It is important to keep in mind that the use of an intra-aortic balloon pump
secondary to decreased ventricular compliance. Bedside ultrasonographic (IABP) is contraindicated. This is because ination of the balloon during
assessment of ventricular volume and inferior vena cava (IVC) diameter diastole will cause massive overload to the left ventricle and aggravate cardiac
variability may provide better assessment tools. decompensation.
c. Avoid acute arterial hypotension. It might precipitate ischemia and cardiac D. Treatment
arrest. An alpha agonist (phenylephrine) is the agent of choice in the setting of 1. Symptomatic patients with severe AR should undergo surgery irrespective of LV
arterial hypotension since it maintains diastolic lling time with a reexively size and function. Patients with severe, chronic AR need medical optimization.
lower heart rate. If a patient has underlying decreased cardiac output (EF< 2. Endocarditis with hemodynamic compromise should prompt urgent surgery.
40%), norepinephrine might be advantageous. Norepinephrine causes a mild to 3. Asymptomatic patients should be followed closely. Surgery is indicated with
earliest signs of decompensation. Chronic mild AR in the perioperative period is disease), chordae tendinae (rupture or elongation), or papillary muscle (rupture or
well tolerated. elongation).
2. Acute MR from ischemia or infarction causes acute LV overload and cardiogenic
Mitral Stenosis (MS) shock (> 50% of patients with MI present some degree of MR).
A. Pathophysiology 3. Chronic MR results in progressive increase in LV compliance followed by
1. Rheumatic heart disease is, by far, the most common cause of mitral stenosis. increase in LVEDV as LV dilates.
Modern early treatment of streptococcus infections has reduced rheumatic disease B. Diagnosis
signicantly, thereby reducing the incidence of mitral stenosis. Rarely, calcium 1. Physical exam ndings include: holosystolic murmur at the apex radiating to the
deposits, malignant carcinoid, lupus or amyloidosis can cause mitral stenosis in axilla, lung rales, and peripheral edema.
adults. It is also a rare congenital defect. 2. TEE is the best technique to determine the degree and nature of MR.
2. Progressive disease causes an enlarged left atrium and atrial brillation. Echocardiography also assesses the status of LV function & provides an estimate
Pulmonary hypertension develops and will become more severe as disease of PA pressures.
progresses. The disease progresses slowly, but acute decompensation can occur C. Management
with increased hemodynamic demands. 1. Treat underlying causes such as uid overload, anemia or infection and optimize
B. Diagnosis preload with diuretics and vasodilators.
1. Physical ndings include a diastolic rumble with an opening snap. 2. Coronary revascularization is indicated for regional wall motion abnormalities
Echocardiography is used for denitive diagnosis and quantication of severity. causing mitral valve apparatus dysfunction.
C. Management 3. For acute decompensation, the pharmacological agents of choice are similar to
1. Perioperative hemodynamic goals for patients with MS: AR (milrinone or dobutamine). In contrast to AR, IABP is an appropriate therapy
a. Maintain sinus rhythm. Supraventricular tachyarrhythmias may precipitate in MR. Diuretics may be considered for treatment of pulmonary edema.
pulmonary edema and cardiovascular collapse. Up to 50% of patients with 4. Perioperative hemodynamic goals for patients with MR are similar to AR
chronic MS develop atrial brillation. patients. However the left ventricle has lower afterload in comparison. Thus
b. Maintain normal cardiac contractility and systemic vascular resistance since left atrial dilation and pulmonary hypertension occurs progressively. Mitral
these patients have a xed cardiac output. The agent of choice in case of arterial regurgitation deteriorates with afterload increase.
hypotension is phenylephrine, because perfusion pressure must be assured and D. Treatment
relative bradycardia secondary to baroreceptor reex might be benecial. 1. Mitral valve repair may be indicated for a prolapsed leaet. Replacement may
c. Identify patients with pulmonary hypertension as a consequence of MS. be indicated if annular morphology does not allow for ring repair.
This subgroup of patients need better management of all factors that worsen 2. Valve resection and replacement is performed for endocarditis with heart failure
pulmonary hypertension (hypoxemia, hypercapnia, acidemia, and hypothermia). to avoid further structural damage.
Some of these patients may present with right ventricular dysfunction. Inotropic 3. Concomitant MAZE may be indicated for paroxysmal AF.
support (epinephrine, milrinone or dobutamine) and judicious uid management
are important in this setting. The use of a pulmonary artery catheter is potentially
helpful to guide the effect of interventions on pulmonary hypertension. Tricuspid Regurgitation (TR)
d. Fluid management in patients with MS mandates careful monitoring. A. Pathophysiology
Suboptimal uid resuscitation decreases cardiac output dramatically and 1. Tricuspid regurgitation is most commonly functional in nature as a consequence
excessive administration of uids will precipitate pulmonary edema and acute of advanced mitral valve disease leading to pulmonary hypertension, RV dilatation
right ventricular failure. and tricuspid annular dilatation. Thus, normal pulmonary arterial pressures
2. Anticoagulation needs to be resumed after risk of postoperative bleeding has are suggestive of structural tricuspid valve disease or primary right ventricular
decreased (usually > 48-72h) in patients who preoperatively had an increased risk dysfunction.
for intracavitary thrombus, i.e. intermittent atrial brillation, large left atrium. B. Diagnosis
D. Treatment 1. Clinical ndings include systolic murmur that increases with inspiration,
1. Procedural intervention is necessary for denitive treatment. Mitral balloon prominent jugular pulsation, and, occasionally, pulsatile liver.
valvuloplasty may be used in specic cases with favorable morphology. C. Management
Otherwise, the valve must be replaced surgically. 1. Perioperative hemodynamic goals for patients with TR and right ventricular
Mitral Regurgitation (MR) a. Maintain appropriate preload. A reasonable goal can be to closely trend the
A. Pathophysiology CVP and maintain it around 15 mmHg. Fluid overload can aggravate TR and RV
1. MR can result from abnormalities of the annulus (dilatation), valve leaets dysfunction.
(myxomatous change, leaet damage from endocarditis, shrinkage from rheumatic b. Maintain adequate RV myocardial perfusion pressure. The RV receives
perfusion both in systole and diastole. It is important to avoid hypotension so
myocardial ischemia is prevented. Questions
c. Decrease RV afterload. Manipulation of all variables that affect pulmonary
vascular resistance is helpful to assure better right ventricular performance 21.1 Which of the following is a perioperative hemodynamic goal for aortic stenosis?
(PaO2, PCO2, pH, hypothermia, and unnecessary use of vasopressors). A. Decrease afterload
B. Limit intravascular volume replacement
d. Maintain normal to high heart rates (> 80s-90s beats per minute). Treat C. Avoid tachycardia
brady-arrythmias aggressively. Low heart rates are inappropriate for state of D. Avoid bradycardia
shock and regurgitation tends to be worse in patients with lower heart rates.
e. Increase RV contractility. Epinephrine or milrinone in combination with 21.2 Which of the following is contraindicated in aortic regurgitation?
A. Tachycardia
norepinephrine are adequate choices for inotropic/vasopressor support in severe B. Afterload reduction
RV dysfunction. C. Intra-aortic balloon pump therapy
D. Treatment D. Surgical correction
1. Repair is indicated for severe TR with mitral valve disease that requires mitral 21.3 Isthe use of a PA catheter sometimes indicated in the management of mitral stenosis?
surgery. Replacement may be considered for cases not amenable for repair. A. No, because it is old technology that has no place in modern ICU practices.
B. No, because the risks outweigh the benets.
C. Yes, because a PA catheter is integral in the management of heart failure that results
from mitral stenosis.
D. Yes, because a PA catheter can assist in the management of pulmonary hypertension,
which may result from mitral stenosis
This chapter is a revision of the original chapter authored by Sriharsha D Subramanya, M.D. and
Jose Diaz-Gomez, M.D.

1. Bonow RO, Carabello BA, Chatterjee K, de Leon Jr AC, Faxon DP, Freed M D, et al:
2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the manage-
ment of patients with valvular heart disease: a report of the American College of Cardiol-
ogy/American Heart Association Task Force on Practice Guidelines Circulation 2008;
2. Moore RA, Martin DE: Anesthetic management for the treatment of valvular heart
disease. A Practical Approach to Cardiac Anesthesia, 3rd ed. Philadelphia, PA, Lippincott
Williams & Wilkins 2003, pp 302-335.
3. Mohan SB, Stouffer, GA: Timing of surgery in aortic stenosis. Current treatment op-
tions in cardiovascular medicine 2006; 8: 421-427.
4. Carabello, BA: The current therapy for mitral regurgitation. J Am Coll Cardiol 2008;
52: 319-326.
5. Gillinov AM, Blackstone EH, Nowicki ER, Slisatkorn W, Al-Dossari G, Johnston DR,
et al. G.: Valve repair versus valve replacement for degenerative mitral valve disease. J
Thorac Cardiovasc Surg 2008; 135:885-893.
6. Bojar RM: Manual of perioperative care in adult cardiac surgery. Wiley-Blackwell,
7. Khot UN, Novaro GM, Popovi ZB, Mills RM, Thomas JD, Tuzcu EM, et al: Nitroprus-
side in critically ill patients with left ventricular dysfunction and aortic stenosis. N Engl J
Med 2008; 348(18):1756-1763.

22. Adult Congenital Heart Disease
Anila Balakrishnan MD and Dawn Nye DO

Key Points A 30-year-old man presents to the ED with progressive shortness of breath
and lower extremity edema. His past medical history is signicant only for
More children born with CHD are reaching
a heart murmur as a child and seasonal allergies. On exam, he is noted
to have a loud holosystolic murmur heard best at the left lower sternal
adulthood border, cyanosis of the skin, clubbing of the ngers, and 2+ pitting edema.
Echocardiography reveals a large ventricular septal defect (VSD) with right
The clinician should know the primary lesion, ventricular hypertrophy and right ventricular systolic pressure (RVSP)
whether the lesion was surgically corrected or estimated to be approximately 121 mmHg.
intervened upon, and if there are any residual
hemodynamic lesions present

Cardiology consultation is warranted for all

ACHD beyond a hemodynamically insignificant
simple shunt

Adult congenital heart disease (ACHD) is becoming more prevalent in the clinical setting as children born
with congenital heart defects are surviving into adulthood. Approximately 0.4-1% of babies are born with
congenital heart disease, and greater than 85% survive into adulthood.1-3 In 2000, the prevalence of adult
congenital heart disease was estimated to be about 2800 adults per 1 million. This is a sign of advancement in
the medical eld over the years, but it also poses a unique new challenge to those providers who may not be
prepared to care for such complex patients in the clinical setting. Although a vast topic, we will present some
basics of managing patients with adult congenital heart disease.

Overview of common ACHD

Various types of classication of ACHD include the following: cyanotic vs. acyanotic; simple, moderate,
severe complexity; and simple shunts, obstructive lesions, regurgitant lesions, complex lesions (this group is
discussed in more detail below).

Simple shunts include unrepaired, hemodynamically signicant shunts. Examples include atrial septal
defects (ASD), ventricular septal defects (VSD, see Figure 22.1), atrioventricular septal defects, patent ductus
arteriosus, and patent foramen ovale (PFOs). Ventricular shunts may require expert consultation and close
hemodynamic monitoring, especially if the patient is undergoing the physiologic changes of a critical care ill-
ness. However, after successful repair, most of these patients do not require specialist care.
A. Management: 2. Pulmonary hypertension
1. Air lters for IVs. IV lines should be completely free from air bubbles. Watch 3. Right heart failure
for paradoxical air embolism.
2. Avoid nitrous oxide Regurgitant lesions
3. Close vigilance for arrhythmias. Septal defects are associated with conduction A. Ebsteins anomaly is a defect where the tricuspid valve is abnormal and sits low in
defects. the right ventricle, with an atrialized right ventricle above the valve. The valves
leaets are restricted which leads to severe regurgitation and right heart failure. If
Obstructive lesions surgically repaired, these patients are at risk for arrhythmias from scar tissue near
A. Coarctation of the aorta involves stenosis of the proximal thoracic aorta. There the conduction system.
B. Marfans syndrome is a genetic disorder of connective tissue, which can lead
to severe dilation of the aorta. It can also be associated with mitral and aortic
C. Tetralogy of Fallot (TOF, Figure 22.2) is a collection of four defects that usually
requires repair in the rst two years of life. However, even if repaired, these
patients can present in the future with right heart failure secondary to pulmonary
insufciency from pulmonic valve repair. The four defects include the following:
1. Ventricular septal defect (VSD)

Figure 22.1 Ventricular Septal Defect (VSD), a type of shunt lesion

are many variants of this lesion, but the most frequently encountered lesion is
at the point of insertion of the ductus arteriosus.4 Severe coarctation presents in
the neonatal period and is repaired within the rst few days of life. Less severe
coarctation can present later in childhood or even in adulthood. Once repaired, with
no evidence of recoarctation, these patients can be treated like normal adults during
times of critical illness. It is important to measure blood pressure in all four limbs
to evaluate for recoarctation; differences should be < 20 mmHg. This will also Figure 22.2 Tetralogy of Fallot, a type of regurgitant lesion
allow the clinician to assess if the left subclavian artery was sacriced during the
procedure. These patients have an increased propensity for hypertension as adults.
B. Left Ventricular/Right Ventricular Outow Obstruction (LVOTO/RVOTO) 2. Overriding aorta
encompasses several stenotic lesions beginning at the anatomic LVOT or RVOT 3. Pulmonary stenosis and RVOTO
and stretching to the descending portion of the aortic arch or pulmonary artery,
respectively. These obstructions can be supravalvular, valvular or subvalvular. 4. Right ventricular hypertrophy
1. Lead to ventricular hypertrophy and subsequently, heart failure
2. Evaluate for heart failure and outow obstruction
C. Congenital mitral stenosis: These patients are at increased risk in unrepaired or
incomplete repair for the following:
1. Atrial arrhythmias

Complex lesions 1. Advantages
A. Transposition of great arteries (TGA) involves malposition of the pulmonary a. Near normal arterial saturation
artery and aorta and may also involve abnormal arrangement of any great vessel, b. Decreased chronic volume overload state
which is referred to as transposition of the great vessels. The standard surgical 2. Disadvantages
TGA repair until the late 1980s was the Mustard or Senning repair, which consisted
of a two-way bafe placed between the right and left atria to redirect blood ow a. Chronic venous hypertension
to the appropriate ventricle. The Mustard procedure utilizes a synthetic material to b. Arrhythmias
create the bafe, whereas the Senning procedure utilizes the patients own tissue. c. Decreased CO at rest and with exercise
Currently, repairs are by arterial switch. Long-term complications of the Mustard/ D. Modied Blalock-Taussig shunt (BT shunt) is temporarily used to direct blood
Senning repairs are as follows: ow to the lungs and improve cyanosis and can be used in the rst stage of the
1. Atrial dilation and heart failure from thinner right ventricle being used as the Fontan procedure. The original surgery involved a branch of subclavian artery or
systemic pump carotid artery, which was separated and attached to the pulmonary artery. Now, an
2. Increased incidence of arrhythmias from scar tissue articial conduit is used to connect subclavian or carotid artery to pulmonary artery.
3. Bafe complications, notably stenosis and leaking
B. Congenitally corrected transposition of great arteries occurs when the heart rotates
abnormally during development leading to the ventricles being reversed. If not Management in the clinical setting:
repaired, these patients have a systemic right ventricle, which increases the risk of Management in the clinical setting requires a thorough understanding of the specic
arrhythmias and early onset heart failure. If repaired by a double switch procedure cardiopulmonary anatomy of ACHD patients and imposes an intellectual challenge for
there is less risk of arrhythmias. However, regardless of repair, these patients may the clinician who cares for this patient population. Specically, the clinician should
have abnormal coronary artery anatomy and are prone to ischemia at younger ages. know the primary lesion, whether the lesion was surgically corrected or intervened
C. Univentricular heart (left or right single ventricle) is a group of disease processes upon, and if there are any residual hemodynamic lesions present. It is imperative to
whose classication has been a controversial subject. Most commonly, it refers to consider how interventions that were undertaken affect the patients current circulation.
a functional single ventricle with a second rudimentary or hypoplastic accessory Furthermore, it is important to understand the patients normals, such as their baseline
ventricle. The AV connection is associated with one ventricular chamber (Figure hemoglobin, baseline oxygen saturation, systemic blood pressure, pulmonary blood
22.3).3 The Fontan procedure is used to palliate the following lesions: tricuspid pressure, and baseline ECG.
atresia, pulmonary atresia, and hypoplastic left heart syndrome. The procedure
entails a two-stage process where venous return is directly connected to pulmonary
arteries without going through the ventricle. Note, in this surgically altered Table 22.1 Acyanotic vs Cyanotic Lesions
circuit, cardiac output (CO) is no longer determined by the heart, but rather by
Acynotic Cyanotic (the 5Ts)
transpulmonary ow.
Ventricular Septal Defect (VSD) Transposition of the Great Arteries (TGA)
Patent ductus arteriosus (PDA) Tetralogy of Fallot
Atrial septal defect (ASD) Truncus arteriosus
AV canal Tricuspid valve abnormalities
Total anomalous pulmonary venous
Other: pulmonary atresia, hypoplastic
left heart, coarctation of the aorta,
Eisenmenger syndrome

Management depends on presence of the following:

A. Shunt, balance between the systemic vascular resistance (SVR) and pulmonary
vascular resistance (PVR) is very important
1. Left-to-right shunt (i.e. ASD, VSD, PDA, BT shunt). Patients are acyanotic,
but are more prone to pulmonary congestion. AVOID high PaO2 and low PaCO2
as they cause pulmonary vasodilation and can worsen pulmonary congestion. In
Figure 22.3 Hypoplastic Left Heart general, the shunt decreases with decreased SVR and increases with decreased
PVR. There are minimal onset time effects on IV medications during procedural lower extremity edema, and narrow pulse pressure
sedation. Examples include: 3. Management:
a. PDA: Patients are more prone to coronary ischemia due to ongoing a. Maintain cardiovascular stability as much as possible. IV drugs take longer to
pulmonary runoff during diastole; a mildly low diastolic BP can lead to coronary reach target areas from prolonged circulatory time.
ischemia. b. Afterload reduction with vasodilators may be necessary to decrease cardiac
b. BT shunt: shunt between subclavian artery and pulmonary artery workload and improve cardiac output.
i. Flow is proportional to SVR; in systemic hypotension, pulmonary blood
ow will decrease E. Arrhythmias are very common. They are often secondary to scarring from
ii. Blood pressure in ipsilateral arm will be decreased, so BP monitoring previous cardiac surgery or due to distention of the atria/ventricles. Supraventricular
should be contralateral to repair arrhythmias are more common and may not respond to traditional medical
2. Right-to-left (i.e. TOF). Results in drop in SaO2 that is refractory to increasing management.
oxygen concentration. It also increases dead space ventilation due to decreased
pulmonary blood ow. IV medications will have a faster onset than usual. Specic considerations in the ICU
A. Renal protection. This is especially important in patients with cyanotic lesions
a. Volume due to compensatory mechanisms; they have hyperviscosity and arteriolar
b. Alpha agonists (i.e. phenylephrine) will increase SVR and reduce shunting vasoconstriction.
c. Beta blockers, will decrease RVOTO 1. Minimize nephrotoxic agents, including caution with IV contrast
2. Maintain renal perfusion pressure (RPP)
B. Pulmonary HTN a. RPP = MAP-CVP
1. Early pulmonary hypertension. Increase in PVR in response to hypothermia, b. Extra vigilance in patients with elevated CVP due to baseline cardiac
stress, pain, acidosis, hypercarbia, hypoxia and elevated intrathoracic pressure. physiology: TOF, Ebsteins anomaly, single-ventricle with Fontan circulation.
2. Chronic pulmonary hypertension, xed. PVR is greater than SVR causing right c. Watch for increased intraabdominal pressures as a mechanism for decreased
to-left shunt. Example: renal perfusion (i.e. ascites, right heart failure).
a. Eisenmenger syndrome = most common reason for cyanosis. These patients
have hypoxemia, myocardial dysfunction and arrhythmias. Management: B. Hepatic dysfunction. Result of chronic elevations in CVP, usually from long-
i. Phlebotomy, if hyperviscosity syndrome present standing heart failure or elevated right heart pressures leading to centrilobular
ii. IV uid to avoid hypotension/dehydration necrosis and brosis. Acute or chronic hepatic dysfunction can develop if the patient
iii. Main goal is to prevent further increase in shunting by increasing SVR and has a low CO or hypoxia. Patients with Fontan circulation are at increased risk and,
decreasing PVR. over time, these patients can develop varices and life threatening gastrointestinal
C. Hypoxemia.
Caused by two main mechanisms in this patient population. Of note, these patients C. Hematology and coagulation
tend to be polycythemic, therefore it is important to ensure adequate hydration. 1. Cyanotic patients are polycythemic with associated iron deciency,
1. Inadequate pulmonary blood ow. Management: thrombocytopenia and platelet dysfunction.
a. Maintain systemic blood pressure 2. Right heart failure leading to liver dysfunction and prolonged PT and increased
b. Minimize factors that will increase PVR bleeding risk.
c. Avoid sudden increases in oxygen demand 3. Fontan circulation leading to increased risk for thrombosis due to stasis within
the repaired pathway and increased factor VIII levels.
2. Mixing of deoxygenated and oxygenated blood. Management:
4. Key management issues
a. Avoid pulmonary vasodilation, which increases cardiac work and decreases
systemic blood pressure. a. Early mobilization
b. Balance systemic ow and pulmonary ow. Do not expect normal SaO2. b. DVT prophylaxis
c. Careful monitoring of coagulation status
D. Ventricular dysfunction
1. Causes: Volume overload (large shunts, valve insufciency), obstructive lesions, D. Pulmonary considerations
cardiac muscle disease, and ischemia 1. Etiology of pulmonary compromise
2. Presentation is variable: examples are weight gain, nausea, bloating, decreased a. Hypoplasia of one lung
appetite, fatigue, tachycardia, tachypnea, pulmonary congestion, hepatomegaly, b. Restrictive lung disease
c. Scoliosis edition. Philadelphia, Lippincott Williams & Wilkins Publishers, 2008, pp 898-1069
5. Allan CK: Intensive care of the adult patient with congenital heart disease. Prog Car-
d. Diaphragmatic paralysis due to prior phrenic nerve injury diovasc Dis 2011; 53:274-280
2. Left heart failure: Patients may benet from positive pressure ventilation (PPV) 6. Baumgartner H, Bonhoeffer P, De Groot NM, de Haan F, Deaneld JE, Galie N, et al:
by increasing cardiac output. ESC Guidelines for the management of grow-up congenital heart disease (new version
2010). Eur Heart J 2010; 31:2915-57
3. Right heart failure: PPV can lead to decrease in right ventricular output due to 7. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, et al:
decreased pressure gradient between great veins and right atrium. In patients with ACC/AHA 2008 guidelines for the management of adults with congenital heart disease.
poor right ventricular function, this can compromise systemic cardiac output. Circulation 2008; 118: 2395-451
8. Perloff JK, Warnes, CA: Challenges posed by adults with repaired congenital heart
4. Fontan without communication between common atrium: disease. Circulation 2001; 103: 2637-43
a. Avoid high PEEP 9. Price S, Keogh B: Adult Congenital Heart Disease: Principles and Management in
Critical Care, Cardiovascular Critical Care. Edited by Grifths M, Cordingley J, Price S.
b. Early extubation when possible Hoboken, NJ, Blackwell Publishing Ltd, 2010, pp 167-92
c. Can consider high frequency jet ventilation and negative pressure ventilation 10. Zaks, JM: Congenital Heart Disease in Adults: Review Questions. Hosp Physician
as alternatives. 2000; 36: 35-36

E. Cardiac Considerations Case Discussion

1. Heart failure: Medical management is mostly supportive with treatment for This patient is showing evidence of Eisenmenger syndrome.
symptoms. Follow AHA guidelines for CHF management. VSDs cause left-to-right shunting, which results in higher
2. Arrhythmias are the most common cause of admissions in this population blood ow and pressure directed towards the lung, leading
accounting for 31%. Onset may be a sign of hemodynamic decompensation. to pulmonary hypertension. Over time, this pulmonary
Catheter ablation results are generally worse in this population. Anti-arrhythmics hypertension will cause scarring of the lung parenchyma
are generally poorly tolerated due to negative inotropic properties and side effects.
and hypertrophy of the myocardium, eventually leading to
3. Sudden cardiac death. Unexplained syncope may be a warning sign. a reversal of the shunt (right to left).7 If this patient had
a. 5 defects are known to have the greatest risk: TOF, TGA, congenitally presented prior to the development of severe pulmonary
corrected TGA, aortic stenosis, and univentricular heart hypertension with Eisenmenger syndrome, his VSD
b. Prevention could have been amenable to repair. With the current
i. Internal cardiac debrillator (ICD) implantation is indicated in ACHD presentation, his main options would be for symptomatic
survivors of cardiac arrest after excluding reversible causes (secondary treatment and/or heart-lung transplantation.
ii. Patients with sustained ventricular tachycardia (VT)
a) Invasive hemodynamic monitoring
b) Aggressive replacement of electrolytes (particularly K+, Mg++)
c) Electrophysiology (EP) evaluation
1) First line treatment is catheter ablation versus surgical resection, if 22.1 Which of the following is the most common reason for admission in the ACHD patient
feasible population?
2) ICD placement if ablation/surgical resection unsuccessful or not pos- A. Congestive heart failure
B. Infection
sible C. Arrhythmia
3) EP testing should be considered in patients with non-sustained VT to D. Myocardial infarction
determine risk of sustained VT 22.2 Which of the following is true?
4) Note: prophylactic anti-arrhythmics are not indicated for asymptomatic A. Repaired simple shunts (ASD, VSD, PDA) require specialist care
patients with isolated premature ventricular contractions (PVCs) B. In a patient with a modied Blalock-Taussig shunt, blood pressure should be measured
in the arm contralateral to the repair
C. In Ebsteins anomaly, patients tend to have tricuspid stenosis
References D. Positive pressure ventilation is benecial in right heart failure and improves cardiac
1. Hamid M, Khan MA, Akhtar MI, Hameedullah, Saleemullah, Samad K, Khan FH: output
Grown up Congenital Heart Disease patient presenting for noncardiac surgery: Anaes-
thetic implications. J Pak Med Assoc 2010; 60(11): 955-9 22.3 All of the following are cyanotic congenital heart lesions, except?
2. Hepburn L, Kelleher A: Grown-up congenital heart disease. Anaesthesia & Intensive A. Tetralogy of Fallot
Care Medicine 2009; 10(9): 451-6 B. Patent ductus arteriosus
3. Khairy P, Poirier N, Mercier LA: Univentricular Heart. Circulation 2007; 115: 800-12 C. Truncus arteriosus
4. Allen H, Driscoll DJ, Shaddy RE, Feltes TF: Part VII: Congenital Cardiovascular D. Transposition of the great arteries
Malformations. Moss and Adams Heart Disease in infants, children and adolescents, 7th

23. Extra-Corporeal Life Support and
Ventricular Assist Devices Mariya Geube MD and Edward A Bittner MD PhD

Key Points A 32 year-old woman is admitted to the ICU with respiratory failure
after aspiration of gastric contents, which occurred during induction of
Extracorporeal life support (ECLS) is a
anesthesia. Her ICU course is complicated by progressively worsening
hypoxemia. Chest radiograph reveals bilateral inltrates consistent with
comprehensive term that describes all ARDS. ARDS-Net ventilation is initiated, diuretics are administered to
manner of extracorporeal support including decrease pulmonary edema, nitric oxide is administered to improve her
oxygenation, carbon dioxide removal and oxygenation. Despite this support, the patients oxygenation further
hemodynamic support. deteriorates. Given the failure of conventional management the decision
is made to initiate venovenous ECLS. Eight days later the patients
Veno-venous cannulation is used for isolated cardiopulmonary function improves to the point that she is successfully
respiratory failure (tissue hypoxia secondary to liberated from ECLS. On ICU day 14, the patient is extubated and a day
hypoxemia), whereas veno-arterial cannulation later transferred out of the ICU.
is used for cardiac failure (tissue hypoxia
secondary to hypoperfusion) with or without
respiratory failure.

Ventricular Assist Devices (VADs) can be

used as a bridge to recovery, bridge to heart EXTRA-CORPOREAL LIFE SUPPORT
transplantation or as a permanent support Extracorporeal life support (ECLS) is the use of a mechanical device to temporarily support heart and/or lung
destination therapy. Conditions that need to function during cardiopulmonary failure, which is potentially reversible, until organ recovery or replacement
be corrected before VAD placement include occurs. In the current literature, ECLS has replaced the older term Extra Corporeal Membrane Oxygenation
(ECMO), which omits reference to inherent additional supporting measures such as hemodynamic support or
patent foramen ovale or atrial septal defect, carbon dioxide removal.
aortic insufficiency, mitral stenosis, ventricular
septal defect and ventricular thrombus. Indications
Refractory cardiogenic shock
Post cardiac arrest cardiopulmonary support
Failure to wean from cardiopulmonary bypass (CPB) after cardiac surgery
As a bridge to recovery, to heart transplantation or to placement of a long term supportive device
Severe hypoxemic respiratory failure in patients with ARDS despite the optimization of ventilatory support
Bridge to lung transplantation or severe primary graft dysfunction after lung transplantation
Hypercarbic respiratory failure with intractable respiratory acidosis

Modes of ECLS
Venoarterial (VA ECLS) Venous-arterial cannulation is used for cardiac failure (tissue hypoxia secondary
to hypoperfusion) with or without respiratory failure

Venovenous (VV ECLS) Supports respiratory function only and requires

native heart function to deliver oxygenated blood to the tissues (it does not provide
hemodynamic support)

ECLS device circuit

The ECLS circuit consists of intravascular cannulas, a blood pump, a membrane
oxygenator, conduit tubing, a heat exchanger and alarms. Access may use a vein and
artery (VA) or two veins (VV).
Vascular access for cannulation,
1. Peripheral ECLS a venous cannula is placed in the femoral vein and an arterial
cannula in the femoral artery appropriate for emergent situations. (Figure 23.1A)
2. Central ECLS a venous cannula in the right atrium and an arterial cannula in
the ascending aorta appropriate in case of failure to wean from CPB during open
heart surgery. Requires sternotomy. (Figure 23.1B)
3. Cervical ECLS a venous cannula is placed in the internal jugular vein and
arterial cannula is placed in the axillary artery (carotid artery in infants). (Figure
- VV ECLS: a double lumen cannula is placed in the superior vena cava (SVC) or
two separate venous cannulas are inserted (femoral vein for drainage and SVC for
infusion). (Figure 23.1D)
Oxygenator works as an articial lung where the blood is saturated with oxygen
and CO2 is removed. Currently used membranes are composed of silicone or hollow- Figure 23.1.ECLS Cannulation Options: A: femoral vein, femoral artery; B: right
ber. It is very important to monitor the oxygenation of pre-oxygenator and post- atrium, aorta; C: internal jugular, axillary (carotid) artery; D: femoral vein, superior
oxygenator blood gas samples to assess the adequacy of the membrane function. vena cava
Tubing system length and diameter determine the blood ow resistance terial pressure, mixed venous oxygen saturation (SvO2), lactate levels, and base excess.
(Poiseuilles law). The degree of hemodynamic support is controlled by changing the pump ow. Dialing
Sweep gas fresh gas is delivered to the membrane oxygenator to allow for gas up the pump ow increases the amount of blood diverted from the heart to the ECLS
exchange. The composition is determined by a blender that mixes air with oxygen in circuit and is an appropriate maneuver in case of tissue hypoperfusion or inadequate
desired proportions. The gas ow rate determines the CO2 clearance, and the pump oxygenation.
blood ow determines the oxygenation.
Blood pump
ECLS increases left ventricular afterload, because the left ventricle ejects against the
- Roller pumps require a reservoir between the venous drainage cannula and the retrograde ow coming from the arterial cannula. With poor left ventricular function,
pump and utilize gravity for drainage into the reservoir. this may cause a complete failure of the left heart with increased left atrial and pulmo-
- Centrifugal pumps most commonly used in ECLS and CPB machines. They nary venous pressures, and result in pulmonary edema or hemorrhage. In this situation,
create high negative pressures in the circuit eliminating the need for drainage by inotropic support and afterload reduction may be benecial.
gravity. Adequate venous return to the heart is required.
Oxygenation of the upper body in peripheral VA ECLS depends on the mixture of the
Physiology of VA ECLS retrograde ow from the arterial cannula and the cardiac output of the left ventricle.
Venous blood is drained from the right side of the heart, circulates through the device When there is preserved cardiac function (e.g. VA ECLS placed for respiratory sup-
pump where gas exchange occurs and is reinfused into the aorta. An important con- port), deoxygenated blood coming from the non-functioning lungs into the left ventricle
sideration is the size of the venous cannula, which should enable a blood ow of at is ejected into the proximal aortic vessels (arteries perfusing heart and brain) causing
least 50-60 ml/kg/min in adults. Central cannulation allows better venous drainage and signicant tissue hypoxia of these organs. Hypoxemia in this situation can be corrected
higher ows and is suitable for patients with higher metabolic requirements such as by maximizing the ECLS ow, by changing the placement of the arterial cannula to the
patients in septic shock. The adequacy of blood ow is assessed by monitoring mean ar- axillary or subclavian artery or by inserting an additional venous cannula into the SVC

to return some of the oxygenated blood to the right atrium. saturation compared with the mixed venous saturation. When the patient is considered
ready for a weaning trial, the pump ow is gradually decreased, while ventilatory sup-
Oxygenated blood returns from the ECLS circuit to the circulation with a saturation of port is optimized and the circuit gas ow is then stopped. Recovery of the lung function
100%, whereas the blood passing through the failing lungs has a saturation of approxi- generally takes longer than recovery of the heart function usually 1 to 3 weeks.
mately 75%. Mixing of oxygenated blood returning from the ECLS oxygenator together
with the poorly oxygenated blood ejected from the left ventricle results in an arterial
saturation that is a proportional average of the two sources of blood. Usually a SaO2 Complications
of 90% is achieved, as measured from an upper extremity arterial line. An increase in Clot formation especially important in VA ECLS, because large and mobile clots in
arterial SaO2 may indicate (1) improvement in native lung function, (2) decreased car- the circuit can result in systemic thrombembolism.
diac output (since most of the blood comes back from the extracorporeal pump) or (3)
increased ECLS ow (if cardiac output is constant). 2 Oxygenator failure detected by worsening of gas exchange in pre and post
membrane blood samples and an increase of the pressure gradient across the
Weaning of ECLS Inotropic support is initiated 12 hours before a weaning trial. ECLS Air embolism may occur if any component of the venous circuit is open to the
blood ow is then gradually decreased, while monitoring the pulsatility of the arterial atmosphere or if there is a tear in the membrane oxygenator.
waveform. Systolic function during the weaning process can be assessed by echocar-
diography. Bleeding full heparinization during ECLS support is required. Potential sites
of bleeding include the gastrointestinal tract, surgical sites (eg: tracheostomy) or
intracranially. ECLS also results in a consumptive thrombocytopenia secondary to
platelet sequestration in the circuit, which may also contribute to bleeding.
Physiology of VV ECLS Cannulation related bleeding, arterial dissection or pseudoaneurysm, limb
Blood is drained from the venous system into the ECLS machine where gas exchange ischemia resulting from arterial cannula malposition or venous congestion of the limb
occurs and then is reinfused back into the venous system. Widely accepted criteria for resulting from the venous cannula.
initiation of VV ECLS include severe refractory hypoxemia with PaO2/FiO2 ratio below Infection
50-80 for at least 6 hours, uncompensated hypercapnea with a pH < 7.15 or excessively
high inspiratory pressures above 35-40cmH2O.3
Ventricular Assist Devices (VADs) are used for mechanical cardiac support in patients
The primary determinants of arterial oxygenation (PaO2) during VV ECLS are the pump facing imminent death due to acute or decompensated chronic heart failure on maximal
ow rate, the patients native lung function and the degree of recirculation (see below). inotropic support. They can be used as a bridge to recovery, a bridge to heart transplan-
While on ECLS, the goal is to provide rest for the native lungs (achieved by reduc- tation or as a permanent support destination therapy. A device that provides support
ing ventilatory parameters: FiO2 30%, respiratory rate 5/min, plateau pressures below to the left ventricle is referred to as an LVAD, to the right ventricle as an RVAD and to
20-25cm H2O).

Recirculation occurs when the drainage and return cannulas are positioned within the
same vessel (e.g. SVC) or when a double lumen venous cannula is used. A portion of
oxygenated blood returning from the ECLS circuit into the major vein is drained back
into the ECLS circuit together with deoxygenated venous blood. Recirculation may re-
sult in signicant arterial hypoxemia. It can be recognized when PO2 of the gas sample
taken before the oxygenator is higher than the PaO2 of the arterial blood. Placing the
drainage cannula in the SVC and the return cannula in the IVC reduces the problem.

Utility of ECLS in ARDS Early studies (1970s-80s) on the use of ECLS in adult
patients with severe ARDS showed very low survival rates (10%). More recent stud-
ies have shown survival rates of 40-60% among selected patients with ARDS managed
with ECLS.4 This improvement has likely resulted from improvements in ventilator
techniques, ECLS circuits, clinical experience, and supportive care. In current practice,
extracorporeal life support is warranted in patients with severe respiratory failure with
an expected mortality risk exceeding 70-80%.

Weaning of ECLS - Signs of improvement in lung function are a reduction in the cir-
Figure 23.2 Schematic Depiction of LVAD Circuit
culatory ow required to achieve the same PaO2 and an increase in the arterial oxygen

both ventricles as a BiVAD. hypoxemia.

Cardiogenic shock following acute myocardial infarction Management of VADs in the Intensive Care Unit
Cardiogenic shock following cardiac surgery Most often patients come to the ICU with VADs placed in an emergent fashion either
Acute heart failure secondary to myocarditis or acute cardiomyopathy after unsuccessful weaning from CPB or due to cardiogenic shock. These patients usu-
Decompensation or progression of chronic heart failure ally have acute end organ injury secondary to the associated low ow state. Despite
improvement in organ function after mechanical support is initiated, mortality of these
Primary graft dysfunction after heart transplantation patients is high, 30-40% survival to discharge. Patients who have VADs placed in elec-
Selection criteria: Cardiac index (CI) < 2.0 L/min/m2; Pulmonary capillary wedge tive fashion have more favorable outcomes.
pressure (PCWP) > 20mmHg; systolic blood pressure (SBP) < 80mmHg with
impaired end organ perfusion while receiving maximal conservative therapy including
intravenous inotropes and intra-aortic balloon pump (IABP). Approximately 30% of patients with left ventricular (LV) failure who undergo VAD
insertion have concomitant right ventricular (RV) failure, but only a small proportion
(~10%) of them require RVAD placement. Unloading the left ventricle along with ino-
Technical considerations tropic support usually improves RV function.
Cannulation sites
- Flow is dened relative to the position of the device: inow cannula directs Vigilant monitoring of intravascular volume is important for optimal VAD function. Hy-
blood from the heart to the device; outow cannula directs blood from the device to povolemia creates sucking effect on the left ventricle, which is potentially detrimental.
the aorta (Figure 23.2). Fluid overload may aggravate right ventricular dysfunction and thus lead to insufcient
- LVAD inow cannula is placed in left atrium or left ventricular apex; outow ow to the left ventricle. Monitoring uid status is challenging and requires consid-
cannula is placed in the ascending aorta eration of the mean arterial pressure, pump ow, and right and left ventricular lling
- RVAD inow cannula is placed in the right atrium; outow cannula is placed in pressures.
pulmonary artery
VAD types based on ow pattern With non-pulsatile devices, pulse pressure is very narrow, often it is absent. Noninva-
- Pulsatile ow devices eject the blood in a pulsatile fashion into the aorta. These sive blood pressure monitoring, using the oscillation method, as well as pulse oxymetry
devices are extracorporeal, require the presence of valves, and valve malfunction is are inapplicable. Arterial line monitoring results in a tracing, which reects the mean
common long term. arterial pressure (MAP). Due to the lack of pulsatile ow, placement of arterial catheters
- Non-pulsatile ow devices these devices are implantable, do not require valves, can be challenging and requires ultrasound guidance.
and use axial or centrifugal pumps creating non-pulsatile (continuous) ow. Table 23.1 Etiology of systemic hypotension in patients with LVAD
Position of the device relative to the body
Etiology Pump ow CVP PCWP CO MAP
- Extracorporeal consist of a bulky machine situated outside the body
- Intracorporeal small and light devices, associated with decreased bleeding and Hypovolemia
infection rate compared with extracorporeal devices. RV failure
VAD failure
Cardiac conditions that require correction before VAD implantation
1. Patent Foramen Ovale (PFO) or Atrial Septal Defect (ASD) impose risk for right Aortic
to left shunt and severe hypoxemia. Insufciency
2. Aortic insufciency results in regurgitant blood ow through the incompetent Sepsis
valve into the left ventricle and then back into the device. This regurgitant ow can CVP: central venous pressure; PCWP: pulmonary capillary wedge pressure; CO:
lead to increased pump ow from recirculation, as well as further left ventricular cardicac output; MAP: mean arterial pressure
overload and dysfunction, while there are signs of systemic hypoperfusion. The aortic Adapted from Reference 6.
valve should be replaced or oversewn prior to implantation
3. Mitral stenosis results in low ow through the inow cannula
4. Ventricular thrombus is common in the left ventricular apex in patients with Complications
poor ventricular function
Bleeding Due to systemic anticoagulation
5. Ventricular septal defect imposes risk for right to left shunt and severe
Inow cannula malposition May result in obstruction and inadequate drainage
Thromboembolic complications Axial ow pumps are associated with a higher

thrombembolic rate. Systemic anticoagulation is of utmost importance.
Infection The risk for device infection increases with time, reaching approximately Questions
25% at 3 months. Typical sites of infection are the driving line as it enters the skin
or the device pocket. Sepsis is the most common cause of death in patients with 23.1 Which of the following conditions needs to be corrected before LVAD placement in a pa-
intermediate and long term VADs. tient with cardiogenic shock?
A. Mitral insufciency
Device malfunction With pulsatile devices the pump applies signicant B. Atrial brillation
backpressure on the inow valve, which typically becomes incompetent after C. Aortic insufciency
about 6 months of use and requires replacement. Non-pulsatile devices have fewer D. Aortic stenosis
components, thus are more durable.
23.2 Blood oxygenation during ECLS is determined by:
A. Sweep gas ow rate
B. Site of the arterial cannulation peripheral versus central
C. Blood ow rate through the ECLS pump
D. Hollow ber versus silicone membrane oxygenator
23.3 For which of the following patients is initiation of ECLS most appropriate?
1. ELSO Guidelines for Cardiopulmonary Extracorporeal Life Support Extracorporeal Life A. 78 yr old male with lung cancer and an obstructive pneumonia with severe hypercapnea
Support Organization, Version 1:1. Ann Arbor, MI, 2009 and acidemia despite optimized mechanical ventilation
2. Dalton H, Garcia-Filion P: Extracorporeal life Support for Cardiopulmonary Failure, B. 43 yr old female with end stage lung disease due to interstitial lung disease awaiting
Principles and Practice of Mechanical Ventilation, 3rd edition. Edited by Tobin M. The bilateral lung transplantation
McGraw-Hill Companies, Inc, 2010, pp 517-542 C. 28 yr old male patient with idiopathic pulmonary hypertension intubated for severe
3. Brodie D: Extracorporeal Membrane Oxygenation for ARDS in Adults. NEJM 2011; hypoxemia, whose pulmonary artery pressures responded well to inhaled nitric oxide
365:1905-14 D. 56 yr old female admitted for large spontaneous intracranial bleeding who sustained
4. Peek GJ: Efcacy and Economic Assessment of Conventional Ventilatory Support Ver- cardiac arrest 72 hours after admission.
sus Extracorporeal Membrane Oxygenation for Severe Adult Respiratory Failure (CESAR):
a Multicenter Randomized Controlled Trial. Lancet 2009; 374:1351-63
5. Beca J, Wilcox T, Hall R: Mechanical Cardiac Support, Cardiothoracic Critical care,
1st edition. Edited by Sidebotham D, McKee A, Gillham M, Levy J. Philadelphia, Butter-
worth-Heinemann, 2007, pp 342-364
6. Sayer G, Naka Y, Jorde U: Ventricular Assist Device Therapy in Advanced Heart Fail-
ure State of the Art, Cardiac Intensive Care. Edited by Jeremias A, Brown D. Philadel-
phia, Saunders, 2010, pp 579-585

Section 6: Gastroenterology & Nutrition


Gastrointestinal Hemorrhage

Nutritional Support

Acute Pancreatitis

Liver Failure
24. Gastrointestinal Hemorrhage
Evan Roller MD, Brian Wessman MD and Thomas J Graetz MD

Key Points A 65 year-old man with a history of atrial brillation experienced a

syncopal episode resulting in a subdural hemorrhage. He underwent a
Although decreasing in incidence secondary
decompressive craniectomy and was extubated on POD #2. Now, on POD
#3, he exhibits altered mental status, hematemesis, tachycardia, and
to prophylaxis, GI bleeding in the ICU can occur hypotension. His most recent hemoglobin from this morning shows a drop
with significant associated mortality. of 5 g/dL
For both upper and lower GI bleeds,
endoscopy remains the initial diagnostic and
therapeutic interventions of choice.

H2RA and PPI are effective for prophylaxis,

but injudicious use has been shown to increase
nosocomial pneumonia and C.Diff infections.

Surgery and/or interventional radiology

should be consulted for refractory bleeding
despite endoscopic therapies. Introduction
Gastrointestinal hemorrhage (GIB) can be the etiology for admission to the intensive care unit (ICU) or may
occur during the course of a hospital stay. Improvement in resuscitation strategies, enhanced endoscopic tech-
niques, and prophylactic use of medications to prevent GIB have improved patient outcomes.

GIB can be divided into an upper GI source (pharynx to the ligament of Treitz) and lower GI source (distal to
the ligament of Treitz). Upper GIB, which occurs more frequently than a lower GIB, can be further divided
into variceal bleeding and non-variceal bleeding. Lower GIB can be divided into small bowel and colonic
sources of bleeding.

Initial management of the patient with a signicant GIB involves securing the airway (if needed) and main-
taining hemodynamic stability. Endoscopy should be performed as soon as the patient is deemed to be stable
in order to allow directed control of the hemorrhage, if the bleeding source can be identied. If ongoing hem-
orrhage persists, other medical treatments, imaging modalities, and surgical options should be explored.

A. General Population
1. Incidence of 50-100 per 100,000 persons per year
2. Frequently leads to ED presentation/evaluation and ICU admission F. Hypotension requiring use of vasopressors
B. Intensive Care population G. Severe head or spinal cord injury (increased ICP increases cholinergic activity)
1. Incidence of 1.5%; appears to be decreasing secondary to increasing use of GI H. History of GI bleeding
prophylaxis, treatment of H. pylori, and early enteral feeding I. Low intragastric pH
2. Clinically overt bleeding occurs in 5%-25% of critically ill patients who did not J. Thermal injury > 35% of body surface area
receive prophylactic therapy1 K. Major surgery (>4 hours)
C. Mortality rates for patients with massive GIB (bleeding resulting in hemodynamic L. High dose corticosteroids (>250mg/day hydrocortisone or equivalent)
instability with signs and symptoms consistent with hemorrhagic shock and
evidence of either hematemesis or hematochezia) range from 20-39%2 M. Acute lung injury
N. Prolonged duration of enteral tube
Causes O. Post transplantation
A. Upper GIB: P. Smoking and alcohol abuse
(Important to exclude other sources of bleeding, such as pulmonary or intranasal)
1. Peptic ulcer disease (H.pylori, NSAID use) Prophylaxis
2. Esophageal and gastric varices (secondary to liver failure) A. Recommended for ICU patients with the following:
3. Mallory-Weiss tears (increased abdominal pressure after vomiting) 1. Coagulopathy (non-iatrogenic; i.e., not due to warfarin, etc.)
4. Gastritis (NSAID use, Crohns) 2. Mechanical ventilation > 48 hours
5. Esophagitis (gastroesophageal reux) 3. History of GI ulceration or bleeding within 1 year
6. Carcinomas (benign or malignant) 4. At least two of the following risk factors: Sepsis, ICU stay longer than 1 week,
7. Stress related mucosal damage occult bleeding lasting at least 6 days, use of more than 250 mg hydrocortisone or
8. Vascular malformations (gastric antral vascular ectasia)
5. Signicant burns
9. Hemobilia (trauma, s/p ERCP, gallstone, inammation)
6. Neurotrauma (including intracranial bleeding from non-traumatic etiologies)
10. Aortoenteric stula
B. Stress ulcer prophylaxis
11. Pancreatic pseudocyst or pseudoaneurysm
1. Optimize hemodynamic status, splanchnic perfusion and oxygen delivery
12. Hemosuccus (bleeding into pancreatic ducts)
2. Enteral nutrition: buffers gastric acid; may provide energy for mucosa; increases
13. Dieulafoy lesion (gastric) secretion of cytoprotective prostaglandins and mucus; increases mucosal
B. Lower Gastrointestinal bleed perfusion; and blunts vagal stimulation.
1. Diverticular disease 3. Avoidance of ulcerogenic medications: corticosteroids; slow release enteral
2. Colitis (ischemic, infectious, Crohns) potassium; and NSAIDS.
3. Hemorrhoids or ssures 4. Pharmacologic agents4
4. Angiodysplasia/ vascular ectasias a. Histamine type 2 receptor antagonists (H2RA): Inhibit H+:K+ ATPase
5. Polyps/ neoplasm exchange pump by binding to H2 receptor on parietal cell resulting in
6. Meckels diverticulum downstream decrease in acid secretion and potassium uptake. Can be
administered enterally or intravenously. Issues include risk of tachyphylaxis
7. Colonic tuberculosis when given intravenously, alterations in drug metabolism (interaction with
8. Aortoenteric stula cytochrome P450 for cimetidine, but not with famotidine or ranitidine),
9. Infectious diarrhea (viral, bacterial, parasites) thrombocytopenia, impaired liver function, and interstitial nephritis. Elimination
10. Dieulafoy lesion (colonic) occurs via the kidneys, therefore, dose needs to be adjusted in patients with renal
11. Brisk UGIB source insufciency. Less likely to be effective in patients with neurotrauma as they do
not inhibit vagally-induced acid secretion.
b. Proton pump inhibitors (PPI): Inhibit gastric acid by forming irreversible
Risk factors disulde bonds with H+:K+ ATPase exchange pump leading to inhibition of
A. Respiratory failure requiring mechanical ventilation for more than 48 hours secretion of H+ by the parietal cell. PPIs can be administered enterally or
B. Coagulopathy (INR>1.5; platelet count <50 x 109/L) intravenously. Issues include abdominal pain, nausea, diarrhea, and alterations
C. Acute renal insufciency in drug metabolism (interaction with cytochrome P450; i.e., reduction in
D. Acute hepatic failure clopidogrel efcacy in patients with CYP2C19 genotype).
E. Sepsis syndrome c. Sucralfate: Basic aluminum salt coats gastric mucosa and forms protective

layer between gastric contents and mucosa without altering gastric pH. Only 4. Place nasogastric tube and start gastric lavage. Obtain laboratory studies (CBC,
administered enterally. Issues include aluminum intoxication in patients with coagulation studies, type and cross, comprehensive metabolic panel)
kidney injury, binding to drugs reducing absorption (digoxin, ciprooxacin, and 5. Administer PPI bolus and follow by infusion to decrease risk of rebleeding.
warfarin), and clotting of enteral feeding tubes. (pantoprazole 80 mg IV bolus then 8mg/hr for 24-72 hours)
d. Antacids: Neutralize gastric acid and inactivate pepsin. Must be administered 6. Mobilization of specialists: gastroenterology, general surgery, and interventional
intragastric Q1-2hours (dose dependent on gastric pH) radiology (depending on underlying cause of bleeding and available resources)
e. Prostanoids: Reduce ability of parietal cells to generate cyclic AMP in B. Procedural Therapies
response to histamine, reducing gastric acid secretion while enhancing mucosal 1. EGD is recommended within 24 hours
defense mechanisms.
a. Establish diagnosis
C. Risks associated with prophylaxis treatment
b. Provide denitive therapy with clips, banding, thermocoagulation, or
1. Increase in nosocomial pneumonia secondary to increased pH (less acid) of sclerosant injection +/- epinephrine
gastric contents resulting in increased bacterial growth
c. Provides information concerning risk of rebleeding
2. Clostridium difcile enteritis shown to be increased in non-ICU patients
receiving PPI or H2RA. d. May be difcult secondary to material in GI tract. Consider promotility agent
e. Sedation required for procedure may result in inability to protect airway.
Diagnosis 2. Balloon Tamponade
A. History a. Sengstaken Blakemore, Minnesota tube, and Linton-Nachlas
1. Hematemesis: Upper GI bleed b. Requires secured airway
2. Melena: Upper GI bleed or ascending colon c. Placement verication per institution protocol
3. Hematochezia: Brisk upper GI bleed (10%) or lower GI bleed (90%) 3. Surgical Management
B. Gastric lavage: Negative if return is bilious AND non-bloody a. Indications
C. Esophagogastroduodenoscopy (EGD), Colonoscopy, capsule endoscopy, double i. Severe hemorrhage not responsive to resuscitation
balloon enteroscopy ii. Failed endoscopic hemostasis and medical management
D. Tagged red cell scans, Meckels scan iii. Coexisting reason for surgery (perforation, obstruction neoplasm)
E. Mesenteric arteriography iv. Consider splenectomy for gastric varices or colon resection for lower GI
F. Barium contrast upper GI series with small bowel follow through, enteroclysis bleeding
G. Laparotomy with intraoperative enteroscopy when all other diagnostic 4. Portosystemic shunts (Transjugular intrahepatic portosystemic shunt)
investigations have failed a. Primarily for recurrent bleeding secondary to upper GI varices
5. Colonoscopy with laser or thermal coagulation
Management and Treatment 6. Angiography with vasoconstrictor administration/embolization
A. Initial resuscitation C. Other considerations
1. Primary survey (Airway, Breathing, Circulation) followed by history and 1. H. pylori screening
physical exam. Continuous monitoring of vital signs 2. Consider octreotide for variceal bleeding
2. Endotracheal intubation for airway protection, if needed 3. Empiric antibiotics for spontaneous bacterial peritonitis prophylaxis in patients
3. Resuscitation: with end-stage liver disease and ascites
a. 2 large-bore peripheral IVs (16G or larger), peripheral rapid infusion catheter
(RIC), or 8.5 Fr (or larger) introducer central venous catheter. Outcome
b. Initially administer isotonic crystalloid to maintain hemodynamic stability A. Rebleeding
c. Administer blood components to maintain hgb 7-9g/dL, correct coagulopathy, 1. Occurs in 10-15% of patients usually in 48 hours
and maintain platelets > 50,000/ L (ideally correcting coagulopathy should not 2. Endoscopic ndings that predict rebleed: active bleeding vessel = 55%; non-
delay endoscopy) bleeding visible vessel = 43%
d. In times of massive bleeding and exsanguination 3. Location of ulcer: Higher incidence on lesser curvature and posterior-inferior
i. Activate massive transfusion protocol, if available wall of duodenum
ii. Consider tranexamic acid (evidence is conicting) 4. Perform EGD again and attempt to achieve hemostasis. Consider interventional
iii. Consider recombinant activated factor VII (evidence in literature radiology if available.
conicting) B. Poor prognostic factors

1. Esophageal varices Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;
2. Coagulopathy with INR >1.3
3. Chronic liver or renal disease
4. Thrombocytopenia (plt <150K), anemia (hgb <10 g/dL)
5. Initial systolic blood pressure <100 mmHg
6. Advanced age
C. Mortality: 5-10%

Future Therapies7
A. Vaccines for H. pylori and hepatitis C
B. Wireless endoscopy capsules
1. Evaluate bleeding in ED
2. With electrocautery to stop bleeding

GIB is a common disease process encountered in the critical care setting. Patients at
risk include those on mechanical ventilation and those with traumatic brain injury. Its
incidence has decreased due to early recognition of risks factors, early enteral nutrition, Questions:
adequate prophylaxis, and improved ICU care. Different imaging modalities, as well
as medical and invasive treatments are available, yet EGD remains the most commonly 24.1 Factors resulting in a reduced incidence of stress gastritis in the ICU setting include:
used diagnostic and therapeutic tool. Rational transfusion of blood products, correction A. Greater awareness of the pathophysiology of the disease
B. Increased use of prophylactic agents
of coagulopathy, and resuscitation with crystalloids are fundamental. The goal of man- C. Early use of enteral feeds
agement is to rst restore hemodynamic stability and then proceed with diagnostic and/ D. Improvement in resuscitation
or more invasive procedures. E. All of the above

24.2 A 65 year old woman, on mechanical ventilation in the ICU, had an episode of bright red
blood output via her NGT 3 days ago. Endoscopy at the time was negative. She is currently
having a recurrence of UGIB with hemodynamic instability. What would be the best next step:
A. Repeat endoscopy
B. Surgical treatment
C. Angiography
References: D. Initiate resuscitation
1. Ali T, Harty R: Stress-Induced Ulcer Bleeding in Critically Ill Patients. Gastroenterol E. Colonoscopy
Clin North Am 2009; 38:245-65
2. Afessa B: Triage of patients with acute gastrointestinal bleeding for intensive care unit 24.3 An 86-year old woman is admitted to the ICU after presenting with hematochezia. An
admission based on risk factors for poor outcome. J Clin Gastroenterol 2000; 30:281-85 EGD is negative. Colonoscopy is unsuccessful due to the presence of large amounts of blood
3. Quenot JP, Thiery N, Barbar S: When should stress ulcer prophylaxis be used in the and stool in the colon. The patient remains hypotensive despite aggressive resuscitation. A
ICU? Curr Opin Crit Care 2009; 15(2): 139-43 mesenteric angiogram showed a bleeding vessel in her transverse colon. Embolization was at-
4. Krag M, Perner A, Wetterslev J, Mller M: Stress ulcer prophylaxis in the intensive tempted, but it was not successful. The next best step in management of this patient is:
care unit: is it indicated? A topical systemic review. Acta Anaesthesiol Scand 2013; A. Subtotal colectomy
57:835-47 B. Administration of DDAVP
5. Manning-Dimmitt LL, Dimmitt SG, Wilson GR: Diagnosis of gastrointestinal bleeding C. Initiation of vasopressin infusion
in adults. Am Fam Physician 2005; 71:1339-46 D. Bolus 300 micrograms of octreotide followed by an infusion
6. Barkun A, Bardou M. Kuipers E, Sung J, Hunt R, Martel M, et al: International con- E. Administration of recombinant factor VIIa
sensus recommendations on the management of patients with nonvariceal upper gastro-
intestinal bleeding. Ann Intern Med 2010; 152:101-13 24.4 A 49-year old alcoholic is admitted to the ICU after developing an UGIB following severe
7. Swain P: Future innovative therapies to treat upper gastrointestinal bleeding. Gastro- retching during a binge drinking episode. After resuscitation, an EGD is performed which shows
intest Endosc Clin N Am 2011; 21:739-47 linear tears on the gastric side of the gastroesophageal junction. The most important aspect of
8. Mihata R, Bonk J, Keville M: Resuscitation of the patient with massive upper gastroin- management is:
testinal bleeding, EM Critical Care, volume 3, number 2. Edited by Gogela-Carson, C. EB A. Expectant observation
Medicine Publsihers, 2013, B. Administration of antiemetics
9. Dworzynski K, Pollit V, Kelsey A, Higgins B, Palmer K, Guidance Development Group: C. Raising the gastric PH
Management of acute upper gastrointestinal bleeding: summary of NICE guidance. BMJ D. Endoscopic thermal coagulation of the tear
2012; 344:e3412. E. Esophageal resection
10. Villanueva C, Colomo A, Bosch A, Concepcin M, Hernandez-Gea V, Aracil C, et al:

25. Nutritional Support
Jeffrey A Katz MD

Key Points A 27 year-old, 84 kg man with no signicant past medical history is

involved in an industrial re. Upon arrival to the ED, he is found to have
Malnutrition is associated with increased
burns over 40% of his body surface area. Initial uid resuscitation is
carried out and he is intubated for potential airway compromise due to
morbidity and mortality, prolonged hospital suspected inhalation injury. You come on service 3 days after his admission
stay, poor immune function and impaired to the ICU and receive this patient from the outgoing resident. He has
wound healing. no enteral access at this point and has been NPO in the 3 days since his
accident. What are your initial nutritional goals for this patient?
The goal of critical care nutrition is to
prevent the complications associated with

Enteral nutrition is preferred to parenteral

nutrition (If the gut works, use it!)

Refeeding syndrome is a potentially

life threatening complication from
hypophosphatemia during the initiation of Nutrition during critical illness presents many challenges to the clinician and is often approached through a
feeding. Phosphate levels must be monitored multi-specialty team that includes physicians, nurses, and nutritionists. The goal of critical care nutrition is
to signicantly improve the outcome of a patients critical illness by preserving lean body mass and avoiding
closely. the negative consequences of malnourishment. Enteral nutrition is always preferred to parenteral nutrition,
however this is mainly determined by the underlying disease process and the functionality of the GI tract.
The goal of this chapter is to provide a basic framework for critical care nutrition and highlight the challenges
that the clinician will face.

A. Denition
1. Protein Calorie Malnutrition: weight loss of > 10-15% of total body weight or body weight < 90%
B. Identication of patients at risk
1. No reliable laboratory method to determine which patients are or at risk of malnourishment
a. Albumin and pre-albumin are unreliable during critical illness
2. Patient history is best determination of nutritional status
a. Unintentional weight loss
b. Prolonged NPO status
c. Prolonged critical illness
i. Patients lose up to 2%/day of muscle mass Composition of Nutrition Supplementation
ii. Nutrition supplementation to prevent muscle loss A. Step 1: Calculate protein-based calories
iii. Safe to assume that these patients are malnourished and require nutrition 1. Daily protein requirement is 1.2-2.0 g/kg/day
support B. Step 2: 15-30% calories from lipid
C. Consequences of malnutrition C. Step 3: Remainder of calories from carbohydrates (30-70%)
1. Increased morbidity and mortality D. Step 4: Evaluate nitrogen balance to assess adequacy of protein-based calories.
2. Prolonged hospital stay 1. Nitrogen balance = nitrogen intake nitrogen losses
3. Impaired tissue function and poor wound healing 2. If negative, then increase protein-based caloric intake
4. Immune suppression and increased risk for infection E. Step 5: Trace Elements, Vitamins, and Other Additives
1. Selenium and vitamins are associated with lower mortality however remains
Basic Metabolic Needs controversial.
There are three basic categories of macronutrients a. Likely little harm and possible signicant benet to trace elements and
- Carbohydrates: 3.4kcal/g vitamins, so often added
- Lipids: 9kcal/g 2. Immune modulating additives have been an active area of nutrition research
- Protein: 4.1kcal/g a. Fish oils and borage oils have been shown to be efcacious in ALI/ARDS
patients (controversial)
Determination of daily caloric need of critically ill patients. i. Positive studies: decreased incidence of infections and pneumonia
A. Harris-Benedict Equation ii. Negative studies: increase in overall mortality
1. Primarily used for non-ventilated patients b. Most trials have been negative and there is insufcient data to recommend
2. Men: B.E.E = 66.5 + (13.75 x kg) + (5.003 x cm) - (6.775 x age) routine administration of glutamine, arginine, or ornithine ketoglutarate.
3. Women: B.E.E. = 655.1 + (9.563 x kg) + (1.850 x cm) - (4.676 x age) c. Glutamine has been associated with increased mortality in multi-system organ
failure patients.
a. B.E.E.= Basal Energy Expenditure
b. kg=weight in kg, cm=height in cm, age=age in years
B. Ireton Jones Equation You calculate his estimated caloric needs, and decide to
1. Primarily used in mechanically ventilated patients begin nutritional therapy. After numerous attempts, you
2. Total calorie need=1784-11(A)+5(W)+244(S)+239(T)+804(B) are only able to get the nasoduodenal feeding tube into the
a. A=age in years, W=weight in kg, S=sex (1=male 0=female) patients stomach. Do you feed into the patients stomach?
b. T=trauma (1=yes 0=no), B=burns (1=yes 0=no) Should you start TPN instead?
C. Mifin-St. Jeor Equation
1. Men: (9.99 x kg) + (6.25 x cm) (4.92 x age) + 5
2. Women: (9.99 x kg) + (6.25 x cm) (4.92 x age) -161
a. kg=weight in kg, cm=height in cm, age=age in years
D. These formulas may underestimate the metabolic needs of patients with certain
Enteral Nutrition
underlying disease processes. A. Enteral nutrition is always preferred to parenteral nutrition if no contra-indications
1. 25% Increase: peritonitis, long bone fractures, mild/moderate trauma
B. Enteral nutrition has decreased complication rates
2. 50% increase: severe infections, multi-system organ dysfunction, severe trauma
1. No difference in mortality has been shown between enteral vs parenteral
3. 100% increase: severe burn (>40% total body surface area) nutrition
E. Simplied daily caloric estimations can also be made based on a patients weight 2. Decreased infection rate in patients on enteral nutrition
and estimated stress level.
C. Advantages
1. Maintenance or minimal stress: 25-30 kcal/kg/day
1. Maintenance of structural integrity of GI tract
2. Moderate stress: 30-35 kcal/kg/day
2. Release of endogenous GI substances such as cholecystokinin, gastrin, and bile
3. Severe stress (e.g. burns): 35-40 kcal/kg/day salts
3. Increases blood ow to intra-abdominal viscera
4. Preserves gut derived immune system including gut associated lymphoid tissue

(GALT) ileus
D. Contra-indications to enteral nutrition 2. Monitoring gastric residual volume for tolerance of tube feeding is controversial
1. Hemodynamic instability a. JAMA 2013: Not monitoring residual gastric volumes during enteral feeding
2. High vasopressor requirement does not lead to more pneumonia
3. High-output enteric stula b. JPEN Guidelines 2009: Should not hold tube feedings unless gastric residual
E. Access for Enteral Nutrition volume is greater than 500cc
1. Naso-enteric tube most common i. Leads to inadequate nutritional support
a. No difference in complications whether gastric or post pyloric feeding tube
b. Caution advised with gastric feedings in patients with gastric pathology Total Parenteral Nutrition
(ie:Gastroparesis, gastric outlet obstruction, gastric stula) A. Advantages of TPN
c. Pancreatitis: Jejunal feeding tube is preferred 1. Ability to provide nutrients to patients who cannot tolerate enteral feeding
2. Surgical Feeding Tubes 2. If severe malnutrition and non-functional GI tract, TPN for 7 days prior to
a. Reserved for patients who require long term enteral access surgery may improve outcomes
b. Percutaneous Gastrostomy Tubes (PEG, G-Tube) B. Disadvantages
c. Jejunostomy Tubes (J-Tube) 1. Risk of systemic infection is much higher
F. Enteral Nutrition Formulas 2. Liver complications include transaminitis, cholestasis, steatosis, steatohepatitis,
brosis, and cirrhosis
1. Numerous formulas available
3. Hyperglycemia:May be the reason why TPN has higher infection risk
2. Disease specic formulas
4. Need for Central Access
3. Typical ICU formula has 1-2 kcal/mL
a. TPN is hypertonic and requires central access
b. Peripheral parenteral nutrition does exist but requires high volume load
You place a nasal feeding tube that ends in the patients c. Single lumen dedicated to TPN to help reduce infectious risk
duodenum. How do you decide at what rate to start his C. Initiation
tube feeds? How do you monitor his tolerance of feeding? 1. The appropriate time frame to start parenteral nutrition remains controversial if a
Is there utility in monitoring gastric residual volumes? patient is not malnourished prior to ICU admission
2. Late parenteral nutrition (8 days) has been shown to be associated with fewer
complications than early initiation (48 hours). NEJM 2011
G. Initiation of enteral feeding
a. Fewer infections, less cholestasis, more ventilator free days, and reduced
1. Radiographic verication of the feeding tube is absolutely necessary. duration of renal replacement therapy
2. Enteral feedings should be started within 24-48 hours of ICU admission, if b. Late TPN group maintained on dextrose containing uids
possible. If hemodynamically compromised, should hold enteral nutrition until
fully resuscitated and stabilized 3. If a patient is expected to be strict NPO for prolonged period of time, it is
reasonable to start TPN early
3. In ICU, presence or absence of atus or bowel sounds is not a requirement for
initiation of enteral feeding D. Monitoring
4. Head-of-bed should be elevated to 30-45 degrees for aspiration precautions 1. Electrolytes including calcium, magnesium, and phosphate
5. Can consider pro-motility agents if necessary 2. Blood glucose
6. EDEN Trial 3. LFTs
a. Compared low volume enteral feeds: 30% goal calories (10-20cc/hr) for six 4. Triglycerides
days then advanced to goal versus starting at 25cc/hr and advancing to goal as 5. Fluid Balance
quickly as tolerated (q2h advances by 25cc/hr)
b. No difference in mortality, ventilator free days, or infections
c. Full feeding group had increased emesis, gastric residuals, use of prokinetic
agents, higher glucose, and more constipation
7. Common practice is to initiate enteral feeds at 30% calorie goal for 24 hours then
increase by 10-15cc/hr every six hours as tolerated
H. Tolerance of Enteral Feeding
1. Patient complaints of pain, gastric distention, atus, radiographic evidence of
5. Altered mental status including gait disturbances and paresthesias
After 10 days on the ventilator, he has been deemed 6. Cardiomyopathy
medically stable such that he can be weaned from E. Monitor serum phosphate levels with repletion often necessary
mechanical ventilation and potentially extubated. On
numerous attempts at weaning, he becomes tachypneic and This chapter is a revision of the previous versions by R. Dean Nava, JR, MD and Gustavo
develops a mild respiratory acidosis necessitating continued Anagaramo, M.D.
mechanical ventilation. What nutritional factors may be
playing into the difculty weaning from the ventilator and
how might you quantify them? REFERENCES/READING LIST
1. American Society for Parenteral and Enteral Nutrition Board of Directors: Clinical
guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients,
Nutrition Monitoring 2009. JPEN 2009; 33(3): 255-9
A. Several nutrition scales used to calculate the nutritional status of patients. 2. Gramlich L, Kichian K, Pinilla J, Rodych NJ, Dhaliwal R, Heyland DK: Does enteral
nutrition compared to parenteral nutrition result in better outcomes in critically ill adult
Parameters used in these scales include laboratory values (albumin, prealbumin, patients? A systematic review of the literature. Nutrition 2004; 20: 843-8
etc.), BMI, stress level, and amount of weight loss. 3. Doig GS, Heighes PT, Simpson F, Sweetman EA, Davies AR: Early enteral nutrition,
B. Metabolic cart provided within 24 h of injury or intensive care unit admission, signicantly reduces mor-
tality in critically ill patients: a meta-analysis of randomized controlled trials. Intensive
1. Calculation of the patients metabolic needs via indirect calorimetry Care Med 2009; 35:2018-27
2. Helps to ensure the patient is not being underfed or overfed. 4. Guglielmi FW, Boggio-Bertinet D, Federico A, Forte GB, Guglielmi A, Loguercio C,
et al: Total parenteral nutrition-related gastroenterological complications. Dig Liver Dis
3. Metabolic carts are highly expensive and not shown to be benecial; not 2006; 38: 623-42
recommended currently by JPEN guidelines 5. Mizock BA: Risk of Aspiration in patients on enteral nutrition: frequency, relevance,
relation to pneumonia, risk factors, and strategies for risk reduction. Curr Gastroenterol
C. The Fick equation Rep 2007; 9: 338-44
1. The amount of oxygen absorbed is equal to the amount of oxygen consumed 6. Bongers T and Grifths, RD: Are there any real differences between enteral feed for-
mulations used in the critically ill? Curr Opin Crit Care 2006; 12:131-5
2. Extrapolated to the amount of carbon dioxide produced. 7. Heyland D, Muscedere J, Wischmeyer PE, Cook D, Jones G, Albert M, et al: A Ran-
3. Patient must be metabolically stable domized Trial of Glutamine and Antioxidants in Critically Ill Patients. N Engl J Med 2013;
368: 1489-97
a. Dynamic conditions such as sepsis, trauma, and burns give inaccurate results. 8. Reignier J, Mercier E, Le Gouge A, Boulain T, Desachy A, Bellec F, et al: Effect of Not
b. End-tidal carbon dioxide per a given time is measured Monitoring Residual Gastric Volume on Risk of Ventilator Associated Pneumonia in Adults
Receiving Mechanical Ventilation and Early Enteral Feeding: A Randomized Control Trial.
c. Using the Fick equation, the amount of oxygen consumed per minute is JAMA 2013; 309(3): 249-256
calculated. 9. Casaer MP, Mesotten D, Hermans G, Wouters PJ, Schetz M, Meyfroidt G, et al: Early
d. Respiratory quotient is calculated versus Late Parenteral Nutrition in Critically Ill Adults. N Engl J Med 2011; 365(6): 506-
i. RQ= CO2 expired / O2 inspired 10. Ziegler TR: Parenteral Nutrition in the Critically Ill Patient. N Engl J Med 2009;
ii. 0.6-0.7 = starvation/underfeeding 361(11): 1088-97
iii. 0.84-0.86 = desired range/mixed fuel utilization
iv. 0.9-1.0 = primarily carbohydrate
v. >1.0 = overfeeding/lipogenesis
4. Overfeeding leads to difculty weaning from the ventilator due to increased
carbon dioxide production

Refeeding Syndrome
A. This potential complication may happen in chronically malnourished patients
B. These patients often have baseline hypophosphatemia
C. As feeds are initiated, there is an increase in serum insulin levels which shifts
phosphate intracellularly and leads to a precipitous decline in serum phosphate
D. Hypophosphatemia with serum levels < 1mg/dL
1. Respiratory failure secondary to diaphragmatic weakness
2. Muscle weakness
3. Rhabdomyolysis
4. Hemolysis
25.1 A patient has been on enteral tube feeds for 24 hours at 30% predicted caloric needs and
the tube feed rate has been increased. A gastric residual of 200cc has been aspirated. What is
your next step?
A. Check an abdominal x-ray for evidence of an ileus
B. Hold tube feeds and re-check gastric residual in six hours
C. Continue current feeding schedule
D. Initiate total parenteral nutrition

25.2 A metabolic cart (indirect calorimetry) is obtained on a patient and the respiratory quo-
tient is calculated to be 1.1. What nutritional maneuver should generally be undertaken rst in
this situation?
A. Nothing; keep nutritional support as it is
B. Increase overall caloric intake
C. Decrease overall caloric intake
D. Increase carbohydrate fraction of nutritional support

25.3 Advantages of enteral feeding include all of the following EXCEPT:

A. Maintenance of GI structural integrity
B. Decrease in GI visceral blood ow
C. Preservation of GI immune function
D. Decrease in infectious risk

25.4 After beginning to provide nutritional support to a chronically malnourished patient, they
develop confusion and dyspnea. The electrolyte disturbance most likely to be involved is:
A. Hyperkalemia
B. Hypokalemia
C. Hypophosphatemia
D. Hyperphosphatemia
E. Hypermagnesemia

26. Acute Pancreatitis
Mariya Geube MD and Edward A Bittner MD PhD

Key Points A 54 year old man with a history of alcohol abuse presents to the
emergency department with severe epigastric pain radiating to his
The majority of patients who present with
back, along with nausea and vomiting for the past 2-3 days. On exam,
he is tachycardic and hypotensive. Laboratory data is notable for
acute pancreatitis have a mild self-limiting elevated amylase and lipase values. A non-contrast abdominal CT scan
disease with a benign clinical course, but 20% shows an enlarged pancreas with a peripancreatic uid collection. After
have severe acute pancreatitis (SAP) with initial aggressive uid resuscitation, the patient remains hypotensive,
local and extra-pancreatic complications. SAP tachycardic, oliguric, and has an altered mental status. His ABG shows
requires ICU admission and is associated with a pH 7.33, PaCO2 25, PaO2 64 on 6L/min oxygen supplementation, with
high morbidity and mortality. a BE of -6.8 and Lactate 3.7. Chest radiograph shows bilateral diffuse
opacications. The patient is intubated and admitted to the ICU.
Infection of necrotic (peri)pancreatic tissue
is present when: (1) gas in the necrotic tissue
is identified on contrast enhanced CT; (2) a
positive gram stain or culture is obtained
with Fine Needle Aspiration (FNA); or (3) a
positive culture is obtained from the initial
necrosectomy/drainage. Etiology
The most common causes of severe acute pancreatitis (SAP) are heavy chronic alcohol consumption and gall-
Indications for surgical intervention in acute stone disease. Other etiologies include trauma, hypercalcemia, hypertriglyceridemia, medications, infections,
pancreatitis are infected (peri)pancreatic and post-ERCP. In 20% of patients, the etiology of SAP is unknown.
necrosis and/or intraabdominal complications,
including hemorrhage, bowel obstruction,
perforated viscus and abdominal compartment Pathogenesis
syndrome. The release of activated pancreatic enzymes leads to auto-digestion of the pancreatic parenchyma resulting
in inamation, microvascular injury, and necrosis. Activated enzymes may also enter the systemic circulation
causing endothelial injury and activation of the inammatory and coagulation cascades resulting in distant
organ damage. Common associated organ dysfunction include shock, acute lung injury and acute respiratory
distress syndrome (ALI/ARDS), and acute renal failure.

The morbidity and mortality in SAP are highest in the rst two weeks of the disease and are determined by
early and progressive development of multi-organ failure.
Classication complications are not often evident in the rst 3-4 days. Local complications should
1. Severity be suspected when, in the course of the disease, there is a recurrence of the abdominal
pain, secondary peak in the pancreatic enzymes, aggravation or development of new
a. Mild acute pancreatitis organ dysfunction, or systemic hypotension. Any of these should prompt immediate
i. No local complications assessment with repeat imaging study (Figure 26.1).
ii. No systemic organ dysfunction 6. Infected necrotic pancreatic tissue is presumed when extraluminal gas is identied
iii. Resolves within one week on CECT, a positive gram stain or culture is obtained from ne needle aspiration
b. Moderately severe acute pancreatitis (FNA), or a positive culture is obtained from the initial necresectomy/drainage5.
i. Presence of local complications 7. Although FNA is the gold standard for diagnosis of infected necrotic pancreatic
ii. Transient systemic organ dysfunction < 48 hours duration tissue, it may miss the infection because it is based on obtaining a small piece of
tissue. Repeat FNA from a different spot increases the sensitivity of the test.
iii. Exacerbation of co-morbid disease
c. Severe acute pancreatitis (SAP)
i. Presence of local complications Table 26.1 CT Severity Index for acute pancreatitis
ii. Persistent systemic organ failure > 48 hours Imaging Points
2. Type Unenhanced abdominal CT scan
a. Interstitial pancreatitis (edematous form) 80% of the cases
b. Necrotizing pancreatitis 20% of the cases Normal Pancreas 0
3. Local complications Enlargement of the pancreas 1
a. An acute peripancreatic uid collection (typically found in interstitial Changes in pancreas and peripancreatic tissue 2
b. An acute necrotic collection dened as an area of non-viable pancreatic or Single uid collection 3
peripancreatic parenchyma in the early stage of the disease before demarcation. The Two or more uid collections 4
mortality rate in patients with this complication is approximately 10% with sterile
necrosis and 25% in cases of infected necrotic pancreatic tissue 3 Contrast enhanced abdominal CT scan (proportion of necrosis)
c. A pancreatic pseudocyst is an organized uid collection enclosed by granulation 0% 0
tissue located outside of the pancreas (homogeneous liquid on CT scan) as a result of <30% 2
persistent leak from the pancreatic duct, usually occurring 4 weeks after disease onset.
d. A walled-off necrosis is a well-organized collection of heterogeneous liquid and 30-50% 4
non-liquid necrosis in a well dened capsule more than 4 weeks after disease onset. >50% 6
e. The term pancreatic abscess has been abandoned in the current classication, Total Score 0-10
replaced by the more contemporary term infected (peri)pancreatic uid collection 2.
Score > 7 predicts high morbidity and mortality
1. Clinico-laboratory diagnosis of acute pancreatitis is based on the classical Management of Severe Acute Pancreatitis
presentation of abdominal pain, nausea, vomiting and markedly elevated pancreatic Guidelines for the management of severe acute pancreatitis (SAP) in the Intensive Care
enzymes (amylase and lipase at least three times higher than the normal limits). Unit have been established by a multidisciplinary international consensus conference 6.
2. There is a lack of correlation between the degree of elevation of the amylase and
lipase, and the clinical severity of the disease. 1. The initial management of SAP is supportive and consists of aggressive uid
3. Organ specic scoring systems have been created to assess the clinical severity resuscitation, adequate pain relief, antiemetics, and prevention and treatment of organ
and prognosis of acute pancreatitis Ranson criteria, Glasgow criteria. For extra- failure.
pancreatic organ injury assessment Acute Physiology and Chronic Health Evaluation 2. Patients with SAP should be admitted to the ICU when they meet conventional
(APACHE II) - is commonly used. criteria for intensive care unit admission.
4. The CT Severity Index for acute pancreatitis (Table 26.1) is the sum of 2 other 3. Antibiotic prophylaxis
scores derived from the initial unenhanced (CT) and contrast-enhanced (CECT) CT a. Infection of necrotic pancreatic tissue is unusual in the rst week of disease
scans 4 onset. It occurs in 40-70% of patients with SAP after 2 weeks and is the leading cause
5. The initial assessment of the severity of acute pancreatitis is based on the clinical of morbidity and mortality.
presentation and the presence or absence of systemic organ failure. A CECT scan b. Conrmation of infection is very important, since there are signicant
or MRI does not need to be obtained immediately after admission because local differences in the prognosis and management of sterile versus infected necrotic tissue.
Distinguishing between the two can be challenging since the systemic inammatory
response syndrome (SIRS) commonly occurs with SAP whether or not infection is 4. Surgical Intervention
present. a.The necessity and timing of surgical intervention in patients with SAP has been
c. Prophylactic antibiotics are not recommended for patients with SAP within studied extensively. Clinical outcomes are improved by delaying surgery more than 4
the rst week of disease onset, although there is some controversy surrounding weeks from disease onset. This delay allows a clear demarcation to develop between
this practice. A recent meta-analysis suggests that prophylactic antibiotic use is not necrotic and non-necrotic tissue. Early intervention carries the risk of seeding the
associated with a signicant reduction in infected necrotic tissue, requirement for sterile necrotic tissue with microorganisms and incomplete debridement with the need
surgery, or mortality. However, there was a signicant reduction in the hospital length for further surgery.
of stay in the group treated with prophylactic antibiotics.7 b. Indications for surgical intervention include: infected necrotic tissue and/or
d. Routine prophylactic antibiotics in patients with SAP have been shown to result intra-abdominal complications including hemorrhage, bowel obstruction, perforated
in a shift of bacterial ora from Gram-negative microorganisms to fungi and Gram- viscus, and abdominal compartment syndrome.
positive microorganisms with the development of multiple drug resistant strains. c. The standard surgical procedure is open transperitoneal or retroperitoneal
e. Signicant clinical deterioration with high suspicion for infection of necrotic necrosectomy (debridement) with placement of large bore drains. With this approach,
tissue (usually after 10-14 days) should prompt initiation of broad spectrum antibiotic viable pancreatic parenchyma may inadvertently be removed resulting in exocrine
therapy. Rapid de-escalation should occur after return of culture data and antibiotics pancreatic insufciency and diabetes mellitus.
may even be discontinued if infection is not conrmed. d. For well-contained, well-dened collections, less invasive techniques including
f. The initial antibiotic therapy should be directed towards Gram-negative bowel percutaneous drainage, endoscopic (transgastric) drainage, and minimally invasive
ora with good penetration into pancreatic tissue (ie, carbapenems, uoroquinolones, retroperitoneal necrosectomy may be used. As compared to the standard surgical
cephalosporins). approach, these techniques offer control of the source of infection without complete
g. There is insufcient data to support the use of selective decontamination of removal of the gland tissue. A step-up technique8 is currently used, in which
the digestive tract (SDD) with nonabsorbable antibiotics for patients with SAP. This percutaneous or endoscopic drainage of the pancreatic uid collection is performed
therapy is currently not recommended. to mitigate sepsis. If there is no clinical improvement, this is followed by minimally
invasive retroperitoneal video-assisted necrosectomy. The advantages of the step-
up technique are a decrease in surgical trauma, less systemic inammatory response
(compared to an open technique), sparing of pancreatic gland tissue, and a decrease in
the incidence of diabetes and postoperative hernias.
e. In acute pancreatitis resulting from obstruction of the common bile duct
(acute biliary pancreatitis), current recommendations support urgent ERCP with
sphincterotomy (within 72 hours of disease onset) for release of the obstruction. In
patients without obstruction who have suspected or conrmed gallstone disease,
cholecystectomy is indicated, but should be postponed until recovery from the

5. Nutrition
a. The need and timing of nutritional therapy for patients with SAP should be
based on the severity of the disease and the nutritional status of the patient.
b. SAP is a hypercatabolic state and early institution of nutrition is crucial to
prevent severe malnutrition.
c. Classical thinking that bowel rest is needed in acute pancreatitis to decrease
enzyme release from the pancreas has been abandoned due to a substantial body of
literature showing that early institution of enteral nutrition is well tolerated with a
resulting reduction in morbidity.
d. For patients with mild to moderate acute pancreatitis, guidelines recommend
slow advancement of their diet within the rst 3 to 4 days of disease onset as tolerated.
e. Enteral nutrition, compared with parenteral nutrition, has been shown to be
associated with a decreased infection rate, length of hospital stay, lower number
of required surgical interventions, and a trend toward decreased mortality.9
Enteral feeding, compared to the parenteral route, is believed to reduce infectious
Figure 26.1 CT Scan abdomen, showing severe acute pancreatitis (SAP) complications from bacterial translocation by improving intestinal blood ow,
resulting in the preservation of the integrity of the gut mucosa and gastrointestinal

associated lymphoid tissue (GALT). Enteral feeding also attenuates the systemic
inammatory response in patients with SAP. QUESTIONS
f. Ideally, enteral nutrition should be instituted after the initial resuscitation
and within 24 hours of admission in patients with SAP. Enteral nutrition may be 26.1 The recommended initial management of acute necrotizing pancreatitis includes all of the
administered in the presence of local pancreatic complications such as stulas, following except
A. Aggressive uid resuscitation
pseudocyst and ascites. B. Oxygen therapy
g. Nasogastric tubes may be used for administration of enteral nutrition. C. Broad spectrum antibiotic therapy
Postpyloric placement is not necessarily required if gastric feeding is well tolerated. D. Analgesic medications
E. Anti-nausea medications
Continuous feeding is preferred over bolus or cyclic administration.
h. Parenteral nutrition should be considered only if attempts to feed the bowel have 26.2 An indication for surgical intervention in a patient with acute pancreatitis is:
failed by day 6 or 7 in a normally nourished patient. A. Moderate or severe acute pancreatitis
i. Immunomodulating formulas (IMF), balanced nutritional formulas B. Presence of (peri)pancreatic necrosis
C. Documented infection of pancreatic tissue from FNA sample
supplemented with substances believed to modulate inammation and improve D. New organ failure in a patient with Severe Acute Pancreatitis
immune function, have been studied in patients with pancreatitis. Some studies E. New onset of fever and increase in WBC count
have suggested that arginine supplemented formulas can exacerbate pancreatitic
inammation, while formulas containing sh oil may have some benet on the 26.3 Which intervention in severe acute pancreatitis has a conrmed morbidity benet
A. Early surgical intervention
infection rate and reduce mortality. B. Prophylactic antibiotics
j. Administration of probiotics has been associated with an increased incidence C. Probiotics supplements
of multi-organ failure in patients with acute pancreatitis and therefore is not D. Early enteral nutrition
E. Bowel rest and parenteral nutrition
k. Semi-elemental/elemental and polymeric formulas are well tolerated with a
similar incidence of pain, ileus, and bloating. Semi-elemental formulas are associated
with decreased weight loss and hospital stay compared to polymeric formulas 10.

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Occur Early or Late in Acute Pancreatitis? Int J Pancreatol. 2000;28(2):91-5
2. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, Tsiotos GG,
Vege SS, Acute Pancreatitis Classication Working Group: Classication of Acute Pancre-
atitis 2012: Revision of the Atlanta Classication and Denitions by International Consen-
sus. Gut 2013;62(1):102-11
3. Swaroop VS, Chari ST, Clain JE: Severe acute pancreatitis. JAMA 2004;291(23):
4. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH: Acute Pancreatitis: Value of CT
in Establishing Prognosis. Radiology 1990;174(2):331-6
5. Dellinger EP, Forsmark CE, Layer P, Levy P, Maravi-Poma E, Petrov MS, Shimosegawa
T, Siriwardena AK, Uomo G, Whitcomb DC, Windsor JA, Pancreatitis Across Nations
Clinical Research and Education Alliance (PANCREA): Determinant-Based Classication
of Acute Pancreatitis Severity. An International Multidisciplinary Consultation. Ann Surg
2012; 256(6):875-80
6. Nathens AB, Curtis JR, Beale RJ, Cook DJ, Moreno RP, Romand, JA, Skerrett SJ,
Stapleton RD, Ware LB, Waldmann CS: Management of the Critically Ill Patient with Se-
vere Acute Pancreatitis. Crit Care Med 2004;32:2524-36
7. Mazaki T, Ishii Y, Takayama T: Meta-analysis of Prophylactic Antibiotic Use in Acute
Necrotizing Pancreatitis. Br J Surg 2006; 93(6):674-84
8. van Santvoort HC, Besselink MG, Bakker OJ, Hofker HS, Boermeester MA, Dejong
CH, van Goor H, Schaapherder AF, van Eijck CH, Bollen TL, van Ramshorst B, Nieuwen-
huijs VB, Timmer R, Lameris JS, Kruyt PM, Manusama ER, van der Harst E, van der
Schelling GP, Karsten T, Hesselink EJ, van Laarhoven CJ, Rosman C, Bosscha K, de Wit
RJ, Houdijk AP, van Leeuwen MS, Buskens E, Gooszen HG, Dutch Pancreatitis Study
Group: A Step-up Approach or Open Necresectomy for Necrotizing Pancreatitis. N Engl J
Med 2010;362(16):1491-502
9. Marik PE and Zaloga GP: Meta-analysis of parenteral nutrition versus enteral nutri-
tion in patients with acute pancreatits. BMJ 2004;328:1407-12
10. Mirtallo JM, Forbes A, McClave SA, Jensen GL, Waitzberg DL, Davies AR, Interna-
tional Consensus Guideline Committee Pancreatitis Task Force: International Consensus
Guidelines for Nutrition Therapy in Pancreatitis. JPEN 2012;36(3):284-91

27. Liver Failure
C Patrick Henson DO

Key Points A 60 year-old, morbidly obese female with a past history of type
2 diabetes, chronic lower extremity cellulitis, and non-alcoholic
Acute liver failure is rare in the developed
steatohepatitis (NASH) causing chronic cirrhosis presents to the ED with
complaints of fever and fatigue.
world; is usually due to viral infection or drug
toxicity; has the potential for recovery, but On assessment, core temperature is elevated at 39.5 C, pulse is 120 bpm,
overall has a high morbidity and mortality. BP is 92/43 mmHg, and oxygen saturation is 93% on 4L nasal cannula.
On examination, she is alert and oriented. She has ascites, and her lower
Chronic liver failure is more common and is extremities are warm and erythematous, with 1+ pretibial edema. Her labs
usually associated with alcohol consumption are notable for:
and Hepatitis B or C.
WBC 14.1 x 109/L
MELD is a score based on INR, bilirubin and Venous lactate 6.5 mg/dL
creatinine, and predicts short term mortality AST 72 IU/L
without liver transplantation
Total bilirubin 9.1 mg/dL
Albumin 2.1 gm/dL
Liver failure has broad systemic effects, Alkaline phosphatase 81 IU/L
with derangements in the neurological, BUN 53 mg/dL
cardiac, pulmonary, renal, hematological and Creatinine 2.84
immunological systems. INR 2.1.

Blood cultures reveal Gram-positive cocci in clusters, which eventually

speciates MSSA. She was transferred to the Medical ICU for management
of severe sepsis. Her respiratory status and mental status declined, and
on hospital day two she was intubated for altered mental status and
hypoxic respiratory failure. She progressed to septic shock, requiring
norepinephrine and vasopressin infusions. Her lactate was persistently
elevated for the duration of her hospital stay. Her WBC continued to rise
to 50, and repeat blood cultures on day four grew out candida albicans.
Her mental status failed to improve with maximal medical and nutritional
support. She became anuric on day ve, even with adequate intracardiac
lling pressures and systemic blood pressure. She was considered for
emergency orthotopic liver transplantation, but given her multi-organ
system failure and in congruence with her wishes, care was withdrawn on
day six.
Diseases of the liver are important causes of ICU admission and contribute greatly to 3. Electrolyte abnormalities, such as chronic hyponatremia.
morbidity and mortality. Chronic liver failure (CLF) is signicantly more common than 4. Severe encephalopathy, however, is less likely, and this suggests severe disease
acute liver failure (ALF), but the latter typically involves a more rapid disease progres- progression.
sion, and necessitates more aggressive treatment.
The goal of much of the treatment of ALF/CLF in the ICU is protection of the non-
ALF is relatively rare, especially in the developed world. Occurring in the absence of hepatic organs. With therapies designed to prevent further deterioration of the other
preexisting liver disease, it is most commonly a result of viral infection or drug toxic- systems, the potential for spontaneous healing improves, and if transplantation is to be
ity. Spontaneous recovery is possible, since cirrhosis and brosis are not present, but performed, the improved health status of the recipient positively affects the short and
barring this, liver transplantation is the only treatment. A rapid disease progression from long-term success of the procedure.
the onset of jaundice to encephalopathy and coagulopathy is characteristic, and the tim-
ing of this progression can affect outcome. Individuals with slower courses (subacute)
are less likely to recover spontaneously, whereas the more rapidly progressing cases Organ-specic therapies
(hyperacute), commonly the result of acetaminophen toxicity, have more potential
for recovery without liver transplantation. Regardless, the prognosis is grim, with high Neurological
mortality rates and diminished quality of life following transplantation. Hepatic encephalopathy (HE) in ALF/CLF is due to decreased metabolism of circulat-
ing neurotoxic compounds, such as ammonia, which leads to swelling of astrocytes and
CLF is more common, especially in the United States. It is typically associated with al- disruption of normal cognitive pathways. In ALF, the condition develops rapidly, and
cohol consumption and viral infection with Hepatitis B or C, but also with medications as such, normal volume regulating mechanisms are overwhelmed. This predisposes to
and fatty liver disease. The disease progression is slow, in contrast to ALF, and sponta- cerebral edema and elevated intracranial pressure. CLF patients typically have a slower
neous recovery is rare. The only denitive treatment for this condition is liver transplan- progression of HE, and cognitive dysfunction may exist without the mechanical changes
tation, although patients can be effectively managed for long periods of time seen in ALF. Also, the development or worsening of HE in patients with either form of
LF may be facilitated by inammation in another part of the body, often due to infec-
Scoring systems have been developed to assist in outcome prediction and treatment of
patients with ALF/CLF. While generalized scoring systems such as the APACHE and
SOFA criteria are benecial in establishing illness severity of patients with liver disease, HE is often reversible with treatment, although in many instances it involves liver
the Kings College Hospital criteria uses markers of hepatic function such as INR and transplantation. If refractory to treatment and without a suitable organ match, intracra-
bilirubin to predict the likelihood that a patient with ALF will survive without trans- nial hypertension can become severe enough that brainstem herniation may occur. The
plantation. This is important, since earlier transplantation carries improved outcomes in strategies for management of HE should focus on controlling the intracranial pressure
patients who will require it. MELD is associated with CLF. The score is based on INR, (quiet environment, sedation if needed, minimizing stimulation, etc.) and monitoring of
bilirubin and creatinine, and aids in prediction of short term mortality without liver dural pressure may be required. Targeting a cerebral perfusion pressure of 50-80 is con-
transplantation. sidered acceptable. Coagulopathy may prevent the placement of an intracranial pressure
monitor. In these cases, clinical signs of increased intracranial pressure should followed
closely. Therapies to reduce ICP such as mannitol and hypertonic saline can be consid-
MELD = 9.57*Scr + 3.78*Tbil +11.2*INR + 6.43 ered, although care should be taken with these to avoid rapid shifts in serum osmolality.

This model has been shown to help in prognosticating acute LF as well, but given the In conjunction with proper nutritional support, elevations in serum ammonia concentra-
possibility of spontaneous recovery, it is less helpful and is used almost exclusively for tions may be managed with lactulose or rifaximin. Polyethylene glycol may be safer
chronic disease. than lactulose, and this is being studied. Rifaximin may be cost-prohibitive; therefore,
lactulose is the treatment of choice. Therapeutic hypothermia does not appear to confer
The clinical presentation of the patient with LF will vary, especially given the rapidity signicant benet in the management of HE and elevated ICP; and, it may contribute to
with which the ALF patient progresses. Multiple organ systems are usually affected. the worsening of coagulopathy.
Patients may be altered or comatose, hypotensive from cardiovascular instability, have
respiratory difculty and/or acute kidney injury, all of which can develop within days to
weeks of initial disease presentation. CLF may present with many of the same clinical Cardiac
problems, but typically these patients are aware of their disease, and have been main- Increased cardiac output is associated with cirrhosis and CLF. Circulating vasodilatory
tained on chronic therapies designed to reduce the burden on their other organ systems. compounds contribute to increased venous capacitance, most notably in the splanchnic
With that said, the cirrhosis that accompanies CLF creates problems that are not associ- circulation; and, this promotes the high-output cardiac state seen in advanced disease.
ated with ALF, such as: While the cardiac output is usually supranormal, the actual ventricular systolic function
1. Portal hypertension, predisposing to splanchnic varices and bleeding, may be depressed. As the disease state progresses, myocardial thickening and diastolic
dysfunction become apparent. In patients with ALF, hypotension may predominate,
2. Pulmonary hypertension, leading to right ventricular dysfunction and pitting given the shock-like state associated with acute disease. Cardiac function in ALF may
be variable, but is less likely to be affected in the same way as the patient with com- hypovolemia and other causes of ATN (nephrotoxins, complications of diabetes, etc.)
pensated cirrhosis. Careful evaluation of the cardiovascular system is recommended have been ruled out, Liver transplantation often reverses this condition, and TIPS can
in patients with LF admitted to the ICU. Vasopressor and/or inotropic therapy may be help. Medical therapies (such as midodrine, octreotide, and vasopressin analogues) that
necessary in either group, depending on the relative complexity of coexisting processes. reduce the gastrointestinal shunting of blood away from the renal circulation may have
Monitoring of intracardiac lling pressures may be indicated, and qualitative assessment benet. Hemodialysis may also be indicated, although may ultimately worsen outcomes.
of ventricular function with echocardiography is useful. There are no specic standard-
ized recommendations for the utility of these devices in LF, separate from traditional Hematology
recommendations. Coagulopathy is one of the hallmarks of decompensated liver disease, and is seen in
both ALF/CLF. While hepatic synthesis of clotting factors is obviously disrupted, plate-
Pulmonary let number and function are also frequently suppressed, as consumptive processes and
splenic sequestration affect the circulating count and function. It is acceptable to allow
Given the acute nature of ALF, the range of potential pulmonary complications is broad the INR to remain elevated and to avoid platelet transfusion. The INR is not a good
and includes: indicator of overall coagulation in liver failure patients as endogenous anticoagulants,
1. Respiratory depression and aspiration secondary to HE, such as antithrombin, protein C, protein S and components of the brinolytic pathways,
2. Pulmonary edema due to aggressive uid resuscitation or cardiac dysfunction, are also reduced. The thromboelastogram may be a better indicator of coagulation and
3. Pneumonia and bleeding risk. Transfusion should be limited except in ongoing bleeding. It is usually
4. ARDS. not necessary to reverse coagulopathy for invasive procedures such as central venous
catheter placement, liver biopsy, and paracentesis; although, it may be necessary for
intracranial pressure monitor placement.
As HE worsens, the need to control the ventilation of patients with either ALF or CLF
becomes more of a priority. Similar standards apply to the management of increased Nutrition
ICP relative to arterial CO2 tension; namely, mild-moderate hyperventilation may be
benecial in the short term to prevent cerebral herniation, but barring that, targeting Metabolic support is important in patients with ALF/CLF. Given the relative risks and
a normal CO2 is preferred. Care should be taken to minimize stimulation and manage benets of enteral and parenteral feeding, it is reasonable to attempt enteral feeds in
patient comfort when intubating and performing procedures on patients with HE. those patients who will tolerate it, although the data is mixed, and both methods provide
some value.
Patients with cirrhosis and CLF are at risk of similar complications once their disease
progresses, but this group is also at risk for the development of pulmonary hypertension. Severely malnourished patients have signicantly worse disease outcomes; thus, early
The pathogenesis of portopulmonary syndrome is attributed to: assessment of nutritional status is important. Chronically ill patients may have neglected
their food intake in the months prior to admission, while acutely ill patients often have
1. Development of the aforementioned cardiac diastolic dysfunction, increased metabolic requirements. At any rate, oral supplementation with calorie counts
2. Hypertension within the portal system, and and replacement of vitamin deciencies are minimal requirements. Parenteral feedings
3. An imbalance of native circulating pulmonary vasoregulatory compounds such as are recommended when oral intake is not adequate (<30-40kcal/kg/day).
prostacylin and thromboxanes.
Signicant pulmonary hypertension, with mPAP above 40-45mmHg, suggests a very The presence of infection in patients with ALF/CLF can often trigger clinical decom-
high perioperative mortality, and as such, liver transplantation may not be offered to pensation, and as such, should be avoided and aggressively treated. While empiric
these individuals. Echocardiography is important in the evaluation of patients with antibiotics are not recommended for all patients, those with advanced encephalopathy,
suspected portopulmonary hypertension, and right heart catheterization may be useful as presence of SIRS or positive cultures should receive antibiotic therapy, ideally tailored
well in select cases to culture data. In addition, patients listed for transplantation may benet from empiric
antibiotic and antifungal therapy, as new infections may cause them to be delisted.
As with other organs, the kidneys are affected in LF. With ALF, the maintenance of sys-
temic perfusion pressure as well as optimization of intravascular uid status are of para-
mount importance. In CLF, renal function may remain stable over time, but can progress
to hepatorenal syndrome, a state characterized by hepatic and renal failure combined
with circulatory abnormalities such as portal hypertension. The alterations in arterial
and venous pressures in the splanchnic and portal circulations promote renal vasocon-
striction and reduced ltration. Common conditions associated with this phenomenon
include drainage of ascites with large volume shifts, bacterial infection, and some medi-
cations. A cirrhotic patient who develops oliguria and has presumed worsening renal
function should be considered to have hepatorenal syndrome once prerenal failure from
1. Stravitz RT. Kramer AH, Davern T et al.: Intensive care of patients with acute liver fail- QUESTIONS
ure: Recommendations of the U.S. Acute Liver Failure Study Group. Crit Care Med 2007;
35 (11):2498-2508 27.1 Which of the following is true of MELD (model of end-stage liver disease) scoring?
2. Findlay JF, Fix OK, Paugam-Burtz C, et al.: Critical Care of the End-Stage Liver Dis- A. Signies the level of hepatocellular injury
ease Patient Awaiting Liver Transplantation. Liver Transpl 2011; 17:496-510 B. Extrahepatic organ systems are not involved in the calculation
3. Rahimi RS, Rockey DC: End-stage liver disease complications. Curr Opin Gastroen- C. Predicts mortality following TIPS procedure
terol 2013; 29:257-263 D. Is only useful when patients have decompensated illness
4. Feltracco P, Brezzi M, Barbieri S, et al.: Intensive Care Unit Admission of Decom- E. Etiology of disease is a factor in the calculation
pensated Cirrhotic Patients: Prognostic Scoring Systems. Transplantation Proc 2011;
5. Trotter, JF: Practical Management of acute liver failure in the intensive care unit. Curr 27.2 What is the new MELD of the patient from the case presentation?
Opin Crit Care 2009; 15:163-167 A. 14
6. Bernal W, Auzinger G, Dhawan A, et al.: Acute Liver Failure.Lancet 2010; 376:190- B. 18
201 C. 25
7. Fikatas P, Lee JE, Sauer IM, et al.: APACHE III Score Is Superior to Kings College D. 33
Hospital Criteria, MELD score and APACHE II Score to Predict Outcomes After Liver E. 45
Transplantation for Acute Liver Failure. Transplantation Proc 2013; 45:2295-2301
27.3 Which is a common etiology of altered mental status in chronic liver failure?
A. Medication reaction
B. Increased intracranial pressure
C. Hyperglycemia
D. Increased ammonia
E. Hypoxia

27.4 Which of the following is the most likely cause of the patients acute renal failure?
A. Portopulmonary hypertension
B. Renal artery stenosis
C. Abdominal compartment syndrome
D. Acute tubular necrosis from vancomycin administration
E. Hepatorenal syndrome

27.5 Why are patients with cirrhosis at high risk for infection?
A. Decreased hepatic synthesis of complement factors
B. Splenic sequestration of leukocytes
C. Splanchnic shunting of blood away from the liver
D. Decreased phagocytic activity of antigen-presenting cells
E. All of the above

Section 7: Renal and Electrolytes


Acute Renal Failure and Renal


Acid-Base Balance

Electrolyte Abnormalities

Fluid Replacement in the ICU

Renal Replacement Therapy

28. Acute Renal Failure and Renal Protection
C Patrick Henson DO

Key Points A 60 year-old man presents to the ICU following a respiratory arrest. He
is postoperative day 4 from a transhiatal esophagectomy. He has had
The kidney provides a way for the body to
diarrhea for the previous three days. His past medical history is notable for
colon cancer and prior nephrectomy for trauma. Upon arrival to the ICU,
filter and excrete waste, maintain electrolyte he is intubated and laboratory studies are sent. Results are shown:
concentrations, control blood acidity, and
regulate blood pressure WBC 30.2 x 109/L
Hemoglobin 19 mg/dL
Maintenance of normal renal function is INR 1.5
dependent on the delivery of an adequate Na+ 139 mmol/L
volume of blood at an appropriate pressure. K+ 5.2 mmol/L
BUN 75 mg/dL
Critically ill patients are at-risk for the Creatinine 2.4 mg/dL
development of AKI

Contrast-induced AKI can be attenuated

by aggressive IV hydration and oral
N-acetylcysteine The healthy kidney provides a way for the body to lter and excrete waste, maintain electrolyte concentra-
tions, control blood acidity, and regulate blood pressure. Even when injured through chronic conditions such
as diabetes mellitus or hypertension, the system is typically able to continue functioning well enough to avoid
serious complications. Syndromes of critical illness place the renal system at extremely high risk of acute
injury, however, and these insults can be substantially more complicated to assess and manage. The acuity of
the changes and the increased mortality and morbidity associated with renal injury in critical illness mandates
a thoughtful and expeditious approach to diagnosis and treatment.

Maintenance of normal renal function is dependent on one major physiologic principle with two components.
The major principle is the delivery of an adequate volume of blood at an appropriate pressure. The mechani-
cal nature of ltration mandates this perfusion pressure to actively lter the plasma, in addition to providing
oxygen to the organ (2 components). Acute kidney injury (AKI) usually occurs as a result of derangements
in these physiologic processes that can result in rapidly progressive deterioration of renal function leading to
difculties in regulation of intravascular volume and pH and electrolyte abnormalities.

Long-term renal complications in outpatients are typically due to chronic hypertension, but acute hypotension
is more of a concern in AKI. At a certain low mean arterial pressure (MAP), intrinsic autoregulatory process-
es become overwhelmed by perfusion pressure dependency, and the intrarenal blood ow falls off dramati-
cally. While MAP is a good indicator of organ perfusion in the euvolemic patient, hypovolemia and cardiac
insufciency can also worsen renal function through a direct decrease in renal blood ow. As catecholamine
output increases to maintain normal MAP, the compromised patient will shunt blood and urine output as implicit measurements of renal function. Hallmarks of diagnosis
ow from the renal system, and AKI often follows. Systemic shock of any kind is the include a rapid time course, usually less than 48 hours, rise in serum creatinine con-
biggest single risk factor associated with the development of AKI. centration by at least 0.3 mg/dL, and oliguria (UOP < 0.5cc/kg/hour) of at least 6 hours
duration. The early stages of AKI in both sets of criteria suggest less severe injury, but
The physiologic principle of perfusion is important enough to warrant the optimization progression to the later stages is inevitable without resolution of the insult. Early rec-
of its components, pressure and ow, in the face of any renal insult. In addition to the ognition, therefore, is extremely important. Mortality is signicantly increased among
shock states, however, other factors associated with critical illness signicantly increase patients in all stages.
the risk of AKI, such as sepsis, use of vasopressors, vascular embolic events, mechani-
cal ventilation, and nephrotoxic medications. As might be expected, exposure to All currently accepted diagnostic criteria for AKI rely on measurements that have high
surgery is strongly associated with AKI, but studies have demonstrated that as many as variability in patients, especially those with critically illness: urine output and serum
one-third of patients who develop AKI have some degree of renal dysfunction prior to creatinine. Total body water, diuretic use, nutritional status and body mass all confound
admission. It is fairly easy to predict that the diabetic patient with known aortic athero- one or both of these values, causing inappropriate or delayed diagnosis of AKI. This is
sclerosis who presents to the ICU on high-dose vasopressors following laparotomy for especially true of serum creatinine, which has long been considered the gold standard
colonic perforation will be at extremely high risk for development of AKI. As we will for evaluation of glomerular ltration rate (GFR) and renal function. A recent study
see, the current challenges involve discriminating between individuals in the intermedi- suggested that increases in creatinine could be delayed by 24 hours or more in patients
ate risk category, and management of these cases, once risk has been established. with increased uid accumulation, confounding the diagnosis in patients receiving
large quantities of intravenous uids. Novel biomarkers such as neutrophil gelatinase-
Diagnostic criteria have been validated to dene the continuum of AKI. RIFLE, and its associated lipocalin (NGAL), cystatin C and interleukin-18 may be useful as markers of
subsequent modication, AKIN, provide a quick bedside tool to assess for the presence injury, but their use is not yet widespread. In the majority of patients, however, when
and severity of AKI. (Figure 28.1) Both use absolute serum creatinine concentrations the appropriate clinical suspicion is combined with accurate data, patients at risk should

Figure 28.1 AKIN vs RIFLE criteria for kidney injury

be identied with reasonable success. these would be expected to help improve blood ow to the kidneys. In volume overload
states, diuretic therapy may reduce venous pressure with resultant increase in tissue
AKI can be classied as prerenal, postrenal, or intrinsic; simplistic terms that allow us blood ow. However, although these agents can augment urine output, they may also
to contextually frame the mechanism of injury, which helps guide appropriate manage- worsen prerenal AKI. Diuretic therapy should be initiated with caution in AKI states.
ment. Fractional excretion of either sodium or urea (Figure 28.2) can be calculated after Dopamine is a potent vasoactive agent with vasopressor and inotropic effects while at
assessment of the urine and plasma with low values suggesting decreased circulating low doses, acting as a diuretic. The action of dopamine on the renal system is to pro-
volume and kidneys that are effectively reclaiming sodium in an effort to maintain intra- mote diuresis through increased demand on the kidney, without necessarily increasing
vascular volume. Higher values occur with higher than expected sodium wasting and/or tissue blood supply. Studies have shown that low-dose, or renal-dose dopamine, is
a reduced ability to appropriately concentrate the urine. Additional standard assessment not protective to the kidney and may increase mortality.
of the AKI patient includes investigation of the urine for tubular casts and eosinophils,
suggestive of glomerular injury and drug-induced nephritis, respectively. Many well-known nephrotoxins are currently in use in ICUs around the world. There
are several potential injury mechanisms, including disruption of intrarenal hemody-
Ruling out obstruction to urinary ow and elevated backpressure should be considered namics, crystal formation, and direct tubular injury, among others. Antibiotics such
as this is easily correctable. Hydronephrosis by renal ultrasound may suggest obstruc- as aminoglycosides, uoroquinolones and penicillins are likely the biggest offenders,
tion in the ureter or more distally. In early obstruction, the presentation may be similar but common drugs such as ACE inhibitors, NSAIDs, and statins are also implicated.
to a hypovolemic state, with oliguria and evaluation of the urine revealing low urine Inammatory causes of AKI are the most common and eosinophils will be seen in mi-
sodium and low fractional excretion of sodium. In cases of prolonged obstruction, how- croscopic evaluation of the urine sediment. Stopping the offending agent early enough
ever, damage to the kidney may cause a presentation similar to acute tubular necrosis and providing hemodynamic support may allow the renal system time to heal.
(ATN). In the ICU setting, kinks or clots in the urinary catheter are common and easily
resolvable causes of oliguria, and these should be ruled out rst. The rise in contrast-induced AKI (CI-AKI) parallels the increase in dye-requiring
angiographic studies, like cardiac catheterizations and CT scans. The risk of serious
Medical management strategies should rst address the cause of AKI. Assessment of injury increases with the severity of illness and, therefore, patients with no risk factors
volume status and replacement or support of circulation should be considered to address for AKI are extremely unlikely to develop CI-AKI. However, the critically ill patient
global hypoperfusion. Administration of intravenous uids is typically indicated in the is more likely to require studies such as these and they are also more likely to have
setting of prerenal AKI, although dysfunction of other organ systems should be ruled other risk factors for AKI, placing them at higher risk of injury. The mechanism is not
out, as cardiac and hepatic failure can appear prerenal, yet they require quite different fully understood, but intrarenal vasoconstriction, direct cellular toxicity, and decreased
treatments. In most cases, cost-effective choices such as balanced salt solutions may production of vasodilatory mediators are all implicated.
be preferable to human albumin, while most synthetic starches are no longer recom-
mended. In cases of hemorrhage or anemia, the benet of replacing blood products may The goal in management for CI-AKI is twofold: maintain adequate circulating volume
outweigh the risks of transfusion, and this should be determined on a patient-specic and minimize exposure. Consider alternative imaging studies in patients with AKI or
basis. with signicant risk factors, and avoid repeating contrast doses. Use of iso-osmolar or

In conjunction with replacement of circulating volume, vasopressor support may be

indicated, especially in cases of vasodilatory shock. The long-held belief that 65 mmHg
is an acceptable MAP for renal perfusion has been challenged recently, and a pressure
greater than 75 mmHg may be necessary for prevention of AKI. Even though vasopres-
sor use is a risk factor for the development and worsening of AKI, this association is
likely multifactorial and, regardless, systemic hypotension necessitates aggressive treat-
ment. Norepinephrine infusion is the gold standard, while vasopressin and epinephrine
may have additional benets. Phenylephrine may also help maintain renal perfusion
pressure, but the increased intrarenal vasoconstriction without increase in cardiac output
may be deleterious to the kidney-at-risk. In septic patients, a trend toward worsened re-
nal function was seen with phenylephrine when compared to norepinephrine. However,
maintaining appropriate perfusion pressure takes precedence, and phenylephrine may be
used based on availability.

As discussed above, cardiac causes of poor perfusion, such as low-output states due
to poor contractility or obstruction to forward ow, may initially present with normal
blood pressure. Accurate assessment of cardiac function is critical in patients suspected
of having cardiac dysfunction leading to AKI. Inotropic support with milrinone, epi- Figure 28.2 Fractional Excretion of Sodium and Urea (FENa and FEU)
nephrine, or dobutamine is typically the mainstay of cardiac support, and initiation of
low-osmolar contrast media is associated with lower rates of CI-AKI in patients with
renal dysfunction, so these should be used whenever possible. When contrast must be QUESTIONS
used in patients at risk for AKI, hydration should be initiated prior to the exposure and All of the following questions refer to the patient in the case summary.
continued after the procedure, preferentially by the intravenous route. Balanced salt
solutions are ideal, as well as sodium bicarbonate in D5W, which has been shown to 28.1 Which of the following intravenous uid is preferred for this patient?
have some benet. The known free radical scavenger N-acetylcysteine has a relatively A. Packed red blood cells
benign risk prole and has shown to be benecial in emergent situations. It should be B. Hextend
considered in all patients at high risk for CI-AKI in addition to aggressive hydration. C. Hespan
D. Lactated Ringers
E. Fresh frozen plasma
Ultimately, a percentage of patients will progress to require renal replacement therapy
(dialysis), either in the short or long term. Critically ill patients are more likely to 48 hours later, he is now in septic shock, requiring large
tolerate Continuous Renal Replacement Therapy (CRRT) over conventional intermit- doses of vasopressors to maintain MAP > 60 mmHg and
tent hemodialysis (HD), although there seems to be no consensus on which improves increased ventilatory support to maintain oxygenation. He
mortality. More recent studies do support early initiation of renal replacement therapy is oliguric, making < 10 cc/hour of urine.
with a reduction in length of mechanical ventilation. Early appreciation of worsening
renal function remains critical. 28.2 Which of the following would be considered indications for urgent hemodialysis?
A. ECG changes with K+ > 6.0 mmol/L following appropriate medical therapy
B. PaO2 of 50 mmHg (FIO2 1.0) and chest x-ray with perihilar congestion and Kerley B
References: C. pH < 7.1 and minute ventilation of 20 L/min
D. All of the above
1. Kellum JA, Lameire N, KDIGO AKI Guideline Work Group: Diagnosis, evaluation, and
management of acute kidney injury: a KDIGO summary (Part 1). Crit Care 2013; 17: 204 28.3 Which of the following complications is most likely to be related to AKI?
( A. Pericarditis
2. Lameire N, Kellum JA, KDIGO AKI Guideline Work Group: Contrast-induced kidney B. Metabolic alkalosis
injury and renal support for acute kidney injury: a KDIGO summary (Part 2). Crit Care C. Hypophosphatemia
2013; 17: 205 ( D. Hypercalcemia
3. Gammelager H, Christiansen CF, Johansen MG, Tnnesen E, Jespersen B, Srensen
H.: One-year mortality among Danish intensive care patients with acute kidney injury: a
cohort study. Crit Care 2012; 16: R124 ( His laboratory data eventually show a hyperkalemia and
4. Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morgera S, Schetz M, Tan I, acidosis, with signs of volume overload. Vascular access
Bouman C, Macedo E, Gibney N, Tolwani A, Ronco C; Beginning and Ending Supportive
Therapy for the Kidney (BEST Kidney) Investigators: Acute Renal Failure in Critically Ill is placed and continuous renal replacement therapy is
Patients: A Multinational, Multicenter Study. JAMA 2005; 294: 813-8 initiated. Urine output is zero for the previous 6 hours.
5. Macedo E, Bouchard J, Soroko SH, Chertow G, Himmelfarb J, Ikizler TA, Paganini EP,
Mehta RL, for the Program to Improve Care in Acute Renal Disease (PICARD) study: Fluid
Serum creatinine is 3.1 mg/dL, up from a baseline of 1.4
accumulation, recognition and staging of acute kidney injury in critically-ill patients. mg/dL.
Critical Care 2010; 14: R82 (
6. Ricci Z, Cruz DN, Ronco, C: Classication and staging of acute kidney injury: beyond 28.4 Which of the following parameters is suggestive of AKI by the AKIN criteria?
the RIFLE and AKIN criteria. Nat Rev Nephrol 2011; 7: 201-8 A. Creatinine elevated 1.7 mg/dL above baseline
7. Ghahramani N, Shadrou S, Hollenbeak C: A systematic review of continuous renal re- B. Urine output of zero over 6 hours
placement therapy and intermittent haemodialysis in management of patients with acute C. Absolute value of creatinine of 3
renal failure. Nephrology (Carlton) 2008; 13: 570-8 D. A & B only
8. Badin J, Boulain T, Ehrmann S, Skarzynski M, Bretagnol A, Buret J, Benzekri-Lefevre
D, Mercier E, Runge I, Garot D, Mathonnet A, Dequin PF, Perrotin D: Relation between
mean arterial pressure and renal function in the early phase of shock: a prospective, ex- 28.5 Which of the following is a true statement?
plorative cohort study. Critical Care 2011; 15: R135 ( A. AKI is rarely present in patients prior to ICU admission
R135) B. Patients requiring renal replacement therapy for AKI are more likely to require long-
term dialysis
C. Greater than 50% of patients with AKI require renal replacement therapy
D. The occurrence of contrast-induced AKI is equally common in all ICU patients
E. None of the above

29. Acid-Base Balance
Nahel Saied MBBCh

Key Points A 27 year-old woman is admitted to the ICU for a salicylate overdose.
While in the drugstore, she reported to the clerk that she had ingested 75
Acid-base homeostasis is critical to
325-mg tablets of non-enteric coated aspirin. EMS was called and she was
brought immediately to the hospital. In the ED, she received activated
enzymatic function and metabolism. H+ charcoal and polyethylene glycol. She was then transferred to the ICU
concentration affects protein configuration for close monitoring. Upon her arrival into the ICU, laboratory studies are
leading to alterations in many critical sent. Results are shown below.
metabolic pathways. It also alters the
degree of ionization of many compounds ABG:
thereby affecting their transport across cell pH 7.53, PaCO2 23 mmHg, PaO2 111 mmHg, Base Decit 3.0, Bicarbonate
membranes. 19 mmol/L, Oxygen Saturation 99%
The human body has a vast capacity to Na+ 141 mmol/L, K+ 4.3 mmol/L, Cl- 106 mmol/L, CO2 17mmol/L, Mg+ 2.6
buffer H+ in order to maintain a normal pH. mg/dL, Ca2+ 8.6 mg/dL, Phosphorus 3.0mg/dL, BUN 11mg/dL, Creatinine
Only when those reserves are depleted are
1.25 mg/dL, Glucose 198 mg/dL, Salicylate 70 mg/dL
significant acid-base disturbances observed.

In general, most acid-base disturbances are Overview:

mild and inconsequential. However, they The bodys extracellular uid (1/3 of total body water) contains 40 nanomol/L of hydrogen ion (H+) and is
provide an insight into disease processes that regulated within a narrow range by metabolic, renal and respiratory buffering mechanisms. In general, those
might otherwise be missed and could pose mechanisms are very effective in maintaining pH in the normal range (7.40 0.02) unless one or more of such
mechanisms are impaired by disease process, e.g. renal or respiratory insufciency. Most patients in intensive
grave harm to the right patient. care units will have acid-base disorders related to their baseline medical conditions as well as the current dis-
ease process responsible for their admission to the ICU. One must not forget that many therapies required to
In critically ill patients, acid-base disturbances treat critically ill patients will also result in acid-base disturbances. Treatment with diuretics, administration
tend to be complex with more than one of a wide range of intravenous uids and many others will directly impact acid-base balance and may need
disorder present at any given moment. counter therapies until the normal compensatory mechanisms can restore the balance.
Distinguishing the primary disorder is crucial
Acids, bases and buffering mechanisms
to its proper management.
Acidosis or alkalosis is the process by which the pH changes from the normal neutral point (pH 7.40). One
leads to the state of acidemia (pH < 7.35) while the other leads to alkalemia (pH > 7.45). Despite the clear
difference of denition between -osis and -emia, many clinicians use the 2 terms interchangeably. While
acid-base disturbances occur in all body compartments, plasma, extracellular uid as well as intracellularly,
we will focus on the plasma component for the purpose of analysis and treatment.

Carbonic acid is a weak acid that is critical to understanding the basic acid-base balance. It rapidly and easily
dissociates into its various states to stay in constant equilibrium. The ability of carbonic acid to generate hy-
drogen ion (H+), bicarbonate ion (HCO3-) and carbon dioxide (CO2) makes it a versatile when available.
compound. (Table 29.1) This allows both the lung (through CO2 elimination) and the
kidney (through HCO3- formation and reabsorption) to play a central role in maintaining
acid-base balance and offer an essential and agile buffering capacity. When performing an ABG analysis, one should answer the following
What type of disorder exists? acidosis/acidemia or alkalosis/alkalemia?
Table 29.1 Henderson and Modied Henderson Equations What is the primary disorder? Metabolic or respiratory?
[ H+ ][ HCO3- ] = K1[ H2CO3 ] = K2[ CO2 ][ H2O ]; K=dissociation constant Is the primary disorder acute or chronic?
Are there compensatory mechanisms in play and, if so, are they appropriate?
Since H2CO3 itself is of no clinical interest, we can use: Are there other independent disorders?
[ H+ ][ HCO3- ] = K[ CO2 ][ H2O ]
The following 6-step approach was proposed in the early 1980s and was rened in the
Since H2O is constant in vivo: 1990s. it remains easy to follow and answers the above questions systematically.
Step 1: Is the pH acidemic or alkalemic?
[ H+ ][HCO3- ] = K[ CO2 ]
Step 2: Is the primary disturbance respiratory or metabolic?
Step 3: For a respiratory disturbance, is it acute or chronic?
Utilizing Henrys Law ( [ CO2 ]/PaCO2 = 1/kH; kH=Henrys constant):
Step 4: If a metabolic acidosis exists, determine whether an anion gap is present.
[ H+ ] = (24 x PaCO2)/ [HCO3- ] Step 5: Determine if a secondary metabolic disturbance co-exists with an anion gap
(which is the Modied Henderson equation) acidosis.
Step 6: Assess the degree of compensation by the respiratory system for the primary
Note: Hasselbach combined Hendersons equations with Sorensens pH negative log
transformation. This proved to be difcult to understand and provides no additional
medical information to the analysis. Therefore, for the purpose of this chapter, we
will ignore it and use the modied Henderson equation instead.

While the lung and kidney play a critical role in quick and effective buffering mecha-
nisms through carbonic acid, there are other, less modiable, intracellular buffering
systems that contribute to the bodys buffering capacity. Those include phosphate buf-
fers, intracellular proteins, hemoglobin in erythrocytes, and more importantly bone (up
to 40% of acute acid load buffering)

Acid-base analysis:
There are 2 major approaches to interpretation of the acid-base state: the traditional
bicarbonate approach (HCO3-) and the strong ion difference (SID). While some believe Figure 29.1 Acidemia and Alkalemia
SID may be more sensitive in detecting acid-base disturbances, in most cases, it offers
little, if any, advantage over the traditional HCO3- centered approach. In this chapter,
we will use the HCO3- centered analysis as it is simpler and, for all clinical purposes, is metabolic disturbance.
an accurate method of assessing and treating acid-base disturbances.
It is prudent to always verify the accuracy of numbers reported on the ABG by compar-
Typically, acid-base analysis is performed using a blood gas analyzer. The blood ing the [H+] from the modied Henderson equation. A quick method uses the 2 digits
sample can be arterial or venous (ABG versus VBG). The analyzer directly measures following the decimal point of the pH. By subtracting the 2 digits from 80, the resulting
pH, PaCO2, PaO2, and oxygen saturation while bicarbonate and base excess (BE) values
are calculated. In addition, most blood gas laboratory equipment will also measure ba-
sic electrolytes (Na+, K+, Ca++) and hemoglobin. Again, it is important to recognize that
the HCO3- value provided by the ABG is a calculated value and not directly measured.
Hence, for better accuracy, HCO3- values provided by direct electrolyte analysis tech-
nique using serum and not whole blood should be used for interpretation and analysis

number should equal the results from (24xPaCO2)/HCO3-. Chronic respiratory alkalosis: pH increase = 0.03 x (40 PaCO2)/10
Example: Step 4: For a metabolic acidosis, determine whether an anion gap is present.
ABG: 7.24/49/21/120 A normal anion gap is approximately 10-12 mEq/L. The anion gap is the calculated dif-
H+ = 80-24 = 56 ference between negatively charged (anion) and positively charged (cation) electrolytes,
H+ = (24 x PaCO2)/HCO3- = (24 x 49)/21 = 56 which are measured in routine serum assays.
Which conrms that the reported numbers are correct per Hendersons equation
Anion gap = Na+ - (Cl- + HCO3-)
Step 1: Is the pH acidemic or alkalemic?
The ABG pH deviation from the neutral point (7.40 2) identies the disorder as Since the anions and cations are always in balance to maintain electrical neutrality, the
alkalemic or academic. (Figure 29.1) anion gap reects the unmeasured anion concentration. There are more unmeasured an-
ions than cations (Table 29.2) and hence the normal difference expressed by the simple
equation above.
Step 2: Is the primary disturbance respiratory or metabolic?
This step requires one to determine whether the disturbance affects primarily the arterial The causes of an anion gap acidosis differ from those of a normal or non-anion gap
PaCO2 (respiratory) or the serum HCO3- (metabolic). A respiratory disturbance alters acidosis (discussed in common acid-base disturbance). Except in rare situations, the
the arterial PaCO2 (normal value 40, range 38-42). Go to step 3. A metabolic distur- anion gap determination is an excellent tool for narrowing the list of potential causes of
bance alters the serum HCO3- (normal value 24, range 22-26). a metabolic acidosis. Pay attention to patients with hypoalbuminemia as low levels of
If HCO3- < 22, metabolic acidosis is present. Go to step 4. albumin (e.g. cirrhosis, nephrotic syndrome, malnutrition) reduce the normal anion gap
If HCO3- > 26, metabolic alkalosis is present, is respiratory compensation
adequate? Go to step 6.

Step 3: For a respiratory disturbance, is it acute or chronic?

In respiratory acidosis, CO2 retention occurs with the onset of hypercarbic respiratory
failure. Acute changes will result in a pH reduction of 0.08 for every 10 mmHg rise
of PaCO2. However, in chronic respiratory acidosis, the HCO3- shift mediated by the
kidney (compensation) will result in a lesser degree of pH reduction, only 0.03 per
10 mmHg rise of PaCO2. Respiratory alkalosis results from hyperventilation due to
multitude of reasons (see below) and the same rules apply to pH changes in the oppo-
site direction. It is worth noting that the renal compensation will correct the pH toward
normal but never completely so the pH will always indicate the direction of the primary

Table 29.2 Anion Gap reects unmeasured Anions and Cations

Unmeasured Anions Unmeasured Cations
Proteins 15 mEq/L Calcium 5 mEq/L
(mostly albumin)
Organic acids 5 mEq/L Potassium 4.5 mEq/L
Phosphates 2 mEq/L Magnesium 1.5mEq/L
Sulfates 1 mEq/L
23 mEq/L 11 mEq/L

disturbance unless a complex or mixed disorder exists.

Acute respiratory acidosis: pH decrease = 0.08 x (PaCO2 40)/10
Chronic respiratory acidosis: pH decrease = 0.03 x (PaCO2 40)/10
Acute respiratory alkalosis: pH increase = 0.08 x (40 PaCO2)/10 Figure 29.2 Flow diagram for the approach to an acidosis

and can mask a signicant anion gap metabolic acidosis. bance, usually respiratory in origin. For example:
If the measured PaCO2 is less than the Winters expected range, the patient
Step 5: Determine whether other metabolic disturbances co-exist with an anion gap must have respiratory alkalosis in addition to the metabolic acidosis.
acidosis. If the measured PaCO2 is more than the Winters expected range, the patient
A non-anion gap acidosis or a metabolic alkalosis may exist concurrently with an anion must have respiratory acidosis in addition to the metabolic acidosis. (Figure 29.3)
gap acidosis. This determination requires one to account for the increase in the anion It is important to recognize that the Winters formula does not reliably predict the respi-
gap and determine whether an additional variation in HCO3- exists. If no other metabolic ratory response to a metabolic alkalosis. Hypoventilation is the natural compensatory
disturbance exists, then the corrected bicarbonate would be 24 mechanism for a metabolic alkalosis. However the degree of PaCO2 increase does not
exhibit a linear relationship with the HCO3-. There are 2 general rules one can count on
Corrected HCO3- = measured HCO3- + (anion gap - 12) to predict the respiratory response to a metabolic alkalosis:
1. PaCO2 may increase above normal but not usually > 50-55 mmHg to com-
pensate for a metabolic alkalosis.
If the corrected HCO3- varies signicantly above or below 24, then a mixed or more
complex metabolic disturbance exists. To be more specic, if the corrected HCO3- is 2. Compensation is usually incomplete, i.e, pH will improve toward normal but
greater than 24, a metabolic alkalosis co-exists. If the corrected HCO3- is less than 24 will remain > 7.42.
then a non-gap acidosis co-exists. (Figure 29.2)
Common disturbances:
Step 6. Assess the normal compensation by the respiratory system for a metabolic dis- 1. Respiratory acidosis:
turbance. Usually results from hypoventilation or the inability to eliminate CO2 that is manifested
The respiratory system responds quickly to a metabolic disturbance (especially acidosis) as an elevation of PaCO2 and a drop in pH.
and results in a linear reduction in PaCO2. The Winters formula (Figure 29.3) predicts Examples:
the expected PaCO2 in response to a change in HCO3-. In simple metabolic acidosis, the Central nervous system depression (sedatives, central hypoventilation syndrome)
measured PaCO2 will fall within the range predicted by Winters formula. However, if
the expected PaCO2 falls outside the range, one should expect a mixed acid-base distur- Pleural disease (pneumothorax) or lung disease (COPD, pneumonia)
Musculoskeletal disorders (severe scoliosis, Guillain-Barre, myasthenia gravis)
2. Respiratory alkalosis:
Usually results from hyperventilation that is manifested by a decrease in PaCO2 and a
rise in pH.
Catastrophic CNS event (CNS hemorrhage)
Drugs (salicylates, progesterone)
Pregnancy (especially the 3rd trimester)
Decreased lung compliance (interstitial lung disease)
Liver cirrhosis
Anxiety and/or pain
3. Anion Gap Acidosis
Anion gap acidosis results from the accumulation of metabolic acids resulting in con-
sumption of HCO3- in the presence of an anion gap (AG > 12).
Renal failure (uremia, unsecreted acids)
Medications (INH, salicylates)
Ketoacidosis (diabetic, alcoholic)
Alcohol poisoning (methanol, isopropyl)
Glycols (ethylene, propylene)
Lactic acidosis (sepsis, heart failure)
4. Non-Anion Gap Acidosis
Figure 29.3 Respiratory compensation in metabolic acidosis and mixed disorders
Non-anion gap acidosis (AG < 12) results from the loss of bicarbonate or the addition of

external acid and is manifested by a low HCO3-. an elevated HCO3- and normal PaCO2. This leads us to the diagnosis of an acute meta-
Examples: bolic alkalosis if we are unaware of the history of COPD with chronic CO2 retention.
GI loss of HCO3- (diarrhea) Thus, the medical history is crucial in understanding complex acid-base disorders.
Renal loss of HCO3-
Compensation for respiratory alkalosis Treatment
Carbonic anhydrase inhibitor (acetazolamide) It is very rare for a clinician to treat acid-base disorders without also instituting treat-
ment for the inciting pathology. For example, a patient with an anion gap metabolic
Renal tubular acidosis acidosis secondary to severe sepsis must also receive treatment for the septic shock
Ureteral diversion (restore perfusion and initiate antimicrobial therapy). When manipulating the acid-base
Hyperchloremia state, it is important to keep a few important points in mind:
HCl or NH4Cl infusion, TPN
5. Metabolic Alkalosis 1. Most mild and moderate acid-base disturbances are self-limited and will resolve over
Metabolic alkalosis results from an elevation of serum bicarbonate. time if the inciting pathology is treated.
Examples: 2. Utilize and augment the normal compensatory mechanism when possible. For
example, in a severe metabolic acidosis, one must augment respiratory compensation by
Volume contraction (vomiting, excessive diuresis, ascites) assessing a patients ventilation before resorting to administration of buffering agents.
Hypokalemia (H+ exchange with K+) 3. Mild acidosis while a patient is under stress is likely benecial and rarely of any
Alkali ingestion (bicarbonate) harm. Mild acidosis augments oxygen unloading from hemoglobin and into tissues.
Excess gluco- or mineralocorticoids 4. It is rarely benecial to administer HCO3- to patients with a level above 10 mEq/L.
Recover from massive blood product resuscitation (metabolism of citrate) 5. In situations when the pH is < 7.2, administration of intravenous HCO3- is indicated
6. Mixed and complex disorders as a temporizing measure since severe acidosis could be harmful. Make sure CO2 elimi-
It is rare to nd simple acid-base disorders in the critically ill patient, as many of these nation is optimized and maximized. Giving IV HCO3- without proper ventilation will
patients have signicant chronic diseases with baseline acid-base disturbances. In ad- shift H+ intracellularly; intracellular acidosis (Figure 29.4) is far more dangerous than its
dition, many therapies given to critically ill patients may result in additional alterations extracellular counterpart. Administer HCO3- slowly over time to allow for CO2 elimina-
in their acid-base state, e.g. opioids, diuretics, total parenteral nutrition and continuous tion by the lungs.
gastric suctioning. While one may nd a simple primary disorder early in the course of 6. Severe alkalosis (metabolic or respiratory, pH > 7.6) is as harmful as acidosis and
critical illness affecting an otherwise healthy patient, with progression of the inciting acute treatment may be indicated. After correcting the primary pathology, metabolic
disease and application of needed therapies, the disorder becomes complex and addi- alkalosis may be treated with a short course of carbonic anhydrase inhibitors (acetazol-
tional disorders are added to the acid-base milieu. amide) for 24-48 hours. Respiratory alkalosis however may be difcult to treat espe-
cially if the inciting pathology is not acutely modiable, e.g. catastrophic intracranial
Often it is difcult to understand such complex acid-base states. It can be confusing pathology.
when, for example, a patient could have an anion gap and a non-anion gap acidosis at 7. NaHCO3 is a hypertonic solution with a large Na+ load. Be aware of the acute effect
the same time or a chronic respiratory acidosis and an acute metabolic alkalosis. Only on intravascular volume especially in children and in patients with chronic hypona-
when the etiology of each disorder is appreciated can one understand complex disor- tremia. Intracranial hemorrhage can occur in neonates with rapid administration of
ders. In the rst instance, the patient may have had vomiting due to intestinal obstruc- NaHCO3. Acute hypernatremia in patients with low Na+ levels may result in central
tion (causes non anion gap acidosis) and developed sepsis with hypoperfusion and lactic pontine myelinolysis.
acidosis (anion gap acidosis). In the second instance, a patient with severe COPD and 8. THAM solution is another H+ acceptor and could be used to correct a severe meta-
chronic respiratory acidosis with metabolic compensation (elevated HCO3-) is placed on bolic acidosis when Na+ may be contraindicated. It is a weak buffer compared to
mechanical ventilation with immediate normalization of the PaCO2. The ABG will show NaHCO3 but is less hypertonic.

1. Englehart MS and SchreiberMA: Measurement of acid-base resuscitation endpoints:
lactate, base decit, bicarbonate or what? Curr Opin Crit Care 2006; 12(6): 569-74
2. Kaplan L: Acid-base balance analysis: a little off target. Crit Care Med 2007; 35(5):
3. Ghosh AK: Diagnosing acid-base disorders. J Assoc Physicians India 200; 54: 720-4
4. Koeppen BM: The kidney and acid-base regulation. Adv Physiol Educ 2009; 33(4):
Figure 29.4 Movement of extracellular bicarbonate into the cell resulting in an 5. Gunnerson KJ and Kellum JA: Acid-base and electrolyte analysis in critically ill pa-
intracellular acidosis tients: are we ready for the new millennium? Curr Opin Crit Care 2003; 9(6): p. 468-73
6. Kellum JA: Disorders of acid-base balance. Crit Care Med 2007; 35(11): 2630-6
7. Rastegar A: Clinical utility of Stewarts method in diagnosis and management of acid-
base disorders. Clin J Am Soc Nephrol 2009; 4(7): 1267-74
8. Narins RG and Emmett M: Simple and mixed acid-base disorders: a practical ap-
proach. Medicine (Baltimore) 1980; 59(3): 161-87
9. 29.1 A 52
Kurtz year-oldJ,man
I, Kraut with a history
Ornekian of renal
V, Nguyen MK:failure has ananalysis:
Acid-base ABG showing pH 7.33,
a critique of PaCO 33
the Stewart
andmmHg , and HCO3- 17 mmol/L
bicarbonate-centered What is the
approaches. Amnext best step?
J Physiol Renal Physiol 2008; 294(5): F1009-
31 A. Repeat the test due to an error
B. Administer 100 mEq of NaHCO3
C. Initiate hemodialysis
D. Initiate BiPAP
E. Do nothing

29.2 A 66 year-old woman is admitted with fever and leukocytosis. She is found to have
urosepsis. An ABG obtained for tachypnea shows pH 7.34, PaCO2 35 mmHg, PaO2 78 mmHg,
HCO3- 18 mmol/L, Na+ 141 mmol/L, and Cl- 105 mmol/L. The most appropriate response(s)
after initiating antibiotics is/are:
A. Intubate and initiate mechanical ventilation.
B. Check lactate level as it is likely elevated.
C. Administer 50 mEq of NaHCO3.
D. Increase IV uids and monitor urine output.
E. Both B & D

29.3 A 22 year-old man is brought to the ED by ambulance after being in a minor motor ve-
hicle accident. He states his chest hurts and it is difcult to breath. He has no other complaints.
He is noted to have tachypnea and requires oxygen at 2 L/min to maintain a SpO2 >95%. His
chest x-ray shows multiple left-sided rib fractures with a small pneumothorax. His ABG shows
pH 7.47, PaCO2 31 mmHg, PaO 81 mmHg, and HCO3- 22 mmol/L. What is the next best step?
A. Initiate acetazolamide therapy
B. Administer morphine to control pain and anxiety
C. Place a large bore IV and give 1L of 0.9 NS
D. Perform left thoracostomy to drain pneumothorax

30. Electrolyte Abnormalities
Anna M Allred MD and Sheena M Weaver MD

Key Points A 43 year-old woman with a past medical history of smoking and
hypertension presented to the Neurointensive Care Unit 7 days ago with
Both disorders of electrolyte concentration
a conrmed subarachnoid hemorrhage (Hunt-Hess Grade 3). A 3-mm
left anterior cerebral artery aneurysm was noted on angiography. It was
and improper treatment can cause increased successfully coil-embolized on hospital day 1 without complications. Her
morbidity and mortality. most recent laboratory values include: sodium 130 mEq/L (1 day prior 135
mEq/L); potassium 4.5 mEq/L; chloride 102 mEq/L; BUN 32 mg/dL (1 day
As a general rule, the severity of the prior 29 mg/dL); and creatinine 1.21 mg/dL (1 day prior 1.10mg/dL). Her
symptoms correlates with the severity of the urine output has been increasing over the past 24 hours.
disturbance and the rate at which it developed.

If an error is suspected, there is no harm in

repeating the laboratory analysis in a patient
that is asymptomatic.

Pharmacists can play an important role

in determining the cause and in managing
electrolyte disturbances. INTRODUCTION
Electrolytes are necessary for many metabolic and homeostatic functions such as: nerve signal conduction;
Equations and recommendations are hormone function; muscle contraction; cardiovascular function; maintenance of cell membrane structure and
commonly provided, but cannot replace function; bone composition; and acid-base/uid regulation. Disorders of electrolytes are common in the adult
ICU population. Multiple mechanisms are involved, including: altered absorption and distribution; excessive
clinical judgment and knowledge of the or inadequate administration; alterations in hormonal, neurologic and homeostatic mechanisms; gastrointes-
pathophysiology of electrolyte disorders. tinal losses; altered renal losses; changes in uid status and uid shifts; and as side effects of medication ad-
ministration. Below, disturbances in sodium, potassium, calcium, magnesium, and phosphorus are reviewed.

Sodium (Na+)
Hypernatremia Associated with overall mortality rate of 40-70%.
1. Denition: Na+ > 145 mEq/L
2. Causes see Table 30.1
3. Signs & Symptoms
a. Lethargy
b. Irritability
c. Restlessness
d. Thirst
e. Muscle irritability and spasticity c. Disorientation
f. Hyper-reexia d. Muscle cramps or weakness
g. Seizures e. Depressed reexes
h. Coma f. Hyponatremic encephalopathy (Na+ < 120 mEq/L)
i. Death i. Nausea/vomiting
4. EKG Changes - none ii. Seizures
5.Treatment - See Table 30.1 iii. Coma
a. Achieve normal circulatory volume iv. Death
b. Correct no more than 1-2 mEq/L/hr 4. EKG Changes - none
c. Do not correct more than 15 mEq/L/24 hours 5. Treatment see Table 30.2
d. If > 170 mEq/L do not correct below 150 in the rst 48-72 hours a. Recent and acute onset can be more rapidly corrected and is more likely to be
e. Calculate water decit symptomatic
i. Water decit (in liters) = Total body water x [(serum sodium/140)-1] b. Patients with severe manifestations, active seizures, or respiratory failure, can be
1) Replace rst half of water decit over 24 hours treated with a bolus of 100 mL 3% saline over 10 minutes
2) Replace remainder over following 24 to 72 hours i. Bolus can be repeated 1-2 times and followed by an infusion if symptoms
ii. Replace using D5W or 0.45 % NS
ii. Goal is to raise serum sodium 2 to 4 mEq/L.
6. Monitor Check serum sodium every 2-4 hours if symptomatic; every 6-12 hours
after symptoms resolved c. Chronic hyponatremia should be corrected slowly and is usually not associated
with severe symptoms
d. Calculate sodium decit
Table 30.1 Causes and Treatment of Hypernatremia
i. Sodium decit (mEq) = total body water x (140 serum sodium)
Volume Status Causes Treatment 1. Many use 125 or 130 instead of 140 in the calculation so as not to
Hypovolemia Loss of hypotonic uids: NS or LR for hemodynamic overcorrect
- vomiting instability 2. Correct for hyperglycemia if present; 1.6 mEq of Na/L is added for every
- diarrhea Correct water decit once 100 mg/dL increase of serum glucose above 100
- nasogastric suctioning hemodynamically stable ii. Replace fty percent over rst 24 hours
- osmotic diuresis
- burns/open wounds 1) Do not correct more than 12 mEq/L in 24 hours
- sweat (fever, sepsis) 2) Correct acute hyponatremia at a rate of 1-2 mEq/L/hr
- lungs 3) Correct chronic hyponatremia at rate of 0.5 mEq/L/hr
Isovolemia Diabetes insipidus: CDI: iii. Complete remaining replacement over 48 to 72 hours
- central (CDI) - ADH analog: Desmopressin e. Overcorrection can induce central pontine myelinolysis which can manifest
- Nephrogenic (NDI) NDI:
- remove cause gradually over one to six days after rapid correction. Hypertonic saline at more than
- Thiazide (use with caution) 30 mL/hr increases the risk.
i. Findings include:
Hypervolemia Hypertonic saline (HTS) so- Remove HTS
lutions Restrict sodium 1) Pseudobulbar palsy
Sodium bicarbonate solutions Loop or thiazide diuretic 2) Quadriparesis
Mineralocorticoid excess: Can use hypotonic uids: 3) Seizures
- hyperaldosteronism - 0.225% or 0.45% NS
- D5W 4) Movement disorders
6. Monitor - Check serum sodium every 2-4 hours if symptomatic; every 6-12 hours
Hyponatremia after symptoms resolved
1. Denition: Na+ < 135 mEq/L
2. Causes see Table 30.2 Potassium (K+)
3. Signs & Symptoms Hyperkalemia
a. Headache 1. Denition
b. Lethargy a. K+ > 5.0 mEq/L

vi. Cyclosporin & Tacrolimus
Table 30.2 Causes and Treatment of Hyponatremia
vii. Hypoaldosteronism
Hypotonic Hypovolemic: Hypovolemic: 3. Signs & Symptoms (usually do not develop until K+ > 5.5 mEq/L)
(most - excessive diuresis - normal saline (NS)
common) - hemorrhage - Lactated Ringers (LR) a. Muscle twitching
- diarrhea Isovolemic: b. Nausea
- burns - water restriction c. Cramping
- cerebral salt wasting - loop diuretics (i.e.,
Isovolemic: furosemide 20-40 q6-12h) d. Weakness
- secondary to abnormalities of sodium - hypertonic saline e. Paralysis
wasting and water conservation Hypervolemic: f. Palpitations
- SIADH - diuresis
- adrenal insufciency - treat underlying illness g. Cardiac arrhythmias death
- hypothyroidism 4. EKG Changes
- medication side effect a. Peaked T waves
- secondary to inability to maintain normal b. Widened QRS complexes
volume status c. Prolonged PR interval
- cirrhosis d. Shortened QT interval
- renal failure e. Sinusoid wave pattern
f. Ventricular tachycardia or brillation
Isotonic Hyperlipidemia Correct underlying cause
Hyperproteinemia Discontinue protein-based g. Pulseless electrical activity
uids 5. Treatment
Hypertonic Hyperglycemia: Correct underlying cause a. Discontinue exogenous potassium
- DKA Stop hypertonic solutions b. IV calcium if symptomatic or EKG changes present: 1-2 g calcium gluconate or
- HHS calcium chloride; repeat until EKG changes improve
Hypertonic sodium-free solutions (i.e., c. Promote intracellular shift of potassium ions (these medications will normalize
mannitol) serum potassium levels but WILL NOT affect total body potassium)
b. Life threatening is K+ > 6.5 mEq/L i. 10 units of Insulin with 50-100 g dextrose (D50W)
2. Causes ii. Sodium bicarbonate 50-150 mEq IV
a. Extracellular shift in ions iii. Albuterol inhaled
i. Metabolic acidosis d. Increase the elimination of potassium
ii. Trauma i. Loop diuretics start with 40 mg furosemide (30 minutes to see effect)
iii. Rhabdomyolysis ii. Sodium polystyrene 30-90 g PO or PR (1-2 hours to see effect)
iv. Bowel infarction iii. Emergency dialysis, if life threatening
v. Tumor lysis syndrome 6. Monitor - Check levels frequently, every 2 to 6 hours
vi. Insulin deciency DM
b. Medications Hypokalemia
i. Beta-blockers 1. Denition
ii. Succinylcholine a. K+ < 3.5 mEq/L
iii. Digoxin b. Severe is K+ < 2.5 - 3.5 mEq/L with symptoms
c. Excessive potassium ingestion 2. Causes - usually multifactorial
d. Reduced potassium elimination a. Decreased oral intake
i. Renal failure b. Increased losses
ii. Potassium-sparing diuretics i. Thiazide and loop diuretics
iii. ARB & ACE inhibitors ii. GI losses
iv. NSAIDS 1. Diarrhea
v. Heparin 2. Vomiting

3. NGT drainage a. Ca > 10.2 mg/dL
iii. RRT b. Severe is Ca 13 mg/dL
c. Intracellular shift 2. Causes
i. Metabolic alkalosis a. Malignancy
ii. Catecholamines b. Primary hyperparathyroidism
d. Iatrogenic - Infusion of potassium free uids c. Adrenal insufciency
e. Medications d. Pagets disease
i. Albuterol e. Milk alkali syndrome
ii. Insulin f. Rhabdomyolysis
iii. Theophylline g. Medications
f. Caffeine i. Thiazide diuretics
g. Refeeding a malnourished patient ii. Lithium
h. Hypomagnesemia can cause refractory hypokalemia iii. Vitamin D
3. Signs & Symptoms iv.Vitamin A
a. Weakness 3. Signs & Symptoms
b. Muscle cramps a. Fatigue
c. Respiratory compromise b. Confusion
d. Paralysis c. Anorexia
e. Cardiac arrhythmias d. Arrhythmias
f. Death e. Severe
4. EKG Changes i. Obtundation
a. T wave attening ii. Acute renal failure
b. T wave inversion iii. Ventricular arrhythmias
c. ST segment depression iv. Coma
d. Prolonged PR interval f. Chronic
e. Prolonged QRS complexes i. Nephrolithiasis
f. Presence of U waves ii. Metastatic calcications
5. Treatment iii. Renal failure
a. IV and enteral replacement are both effective; replace IV if symptomatic 4. EKG Changes
b. K+ 3.0 - 3.4 mEq/L start with 20-40 mEq IV potassium a. Bradycardia
c. K+ < 3.0 mEq/L may require as much as 200 mEq of potassium b. Prolonged PR interval
i. Start with 40-80 mEq IV replacement at 10-20 mEq/hr (rate depends on c. Wide QRS complex
peripheral or central access) and recheck level d. Short QT interval
ii. High concentration or rapid infusion of replacement potassium may 5. Treatment
necessitate continuous ECG monitoring; especially if > 40 mEq/hr (rare) a. Mild to moderate hypercalcemia commonly only need hydration
iii. Larger doses in setting of ongoing renal or gastrointestinal losses (rare) b. Severe hypercalcemia needs immediate treatment with hydration; NS at 200-300
d. Restoration of normo-kalemia relies on normo-magnesemia ml/hr
e. Avoid dextrose containing solutions c. After hydration, use loop diuretics to increase renal elimination
f. Monitor acid-base status levels will fall 0.6 mEq/L for every 0.1 increase in pH d. RRT if severe or in renal failure
6. Monitor - Check levels frequently, every 2 to 6 hours 6. Monitor - Check daily calcium levels while in ICU

Calcium (Ca2+) Hypocalcemia

Hypercalcemia 1.Denition
1. Denition a. Ca < 8.6 mg/dL

b. Ionized Ca2+ < 1.1 mmol/L i. Nausea/vomiting
2. Causes ii. Hypotension
a. Hypoalbuminemia iii. Bradycardia
b. Hypomagnesemia iv. Loss of DTRs
c. Hyperphosphatemia c. Severe Mg > 12.5 mg/dL
d. Sepsis i. Respiratory paralysis
e. Pancreatitis ii. Refractory hypotension
f. Hypoparathyroidism iii. Atrioventricular block
g. Vitamin D deciency iv. Cardiac arrest
h. Renal insufciency 4. EKG Changes
i. Citrated blood products a. Wide QRS complex
3. Signs & Symptoms b. Prolonged PR interval
a. Tetany c. Bradycardia
b. Chvostek & Trousseau signs 5. Treatment
c. Altered mental status a. Discontinue magnesium continuing medications
d. Chronic b. 1 g IV calcium to stabilize cardiac membrane (over 5 min)
i. Hair loss c. Loop diuretics
ii. Dermatitis d. Renal replacement therapy
iii. Eczema 6. Monitor check levels daily while correcting
iv. Grooved nails
4. EKG Changes Hypomagnesaemia
a. Prolonged QT interval 1. Denition
b. Bradycardia a. Mg < 1.5 mg/dL
5. Treatment b. Severe is Mg < 1.0 mg/dL
a. Do not need to treat asymptomatic patients 2. Causes
b. For every 1 g/dL decrease in serum albumin below 4 g/dL, the serum calcium a. GI losses
concentration will decrease by 0.8 mg/dL. b. Pancreatitis
c. Treat when Ca < 7.5 mg/dL or ionized Ca++ < 0.9 mmol/L c. Malnutrition
i. IV calcium chloride (13.6 mEq/10 mL) d. Renal losses
ii. IV calcium gluconate (4.56 mEq/10 mL) e. Surgery
1) Start with 1-3 g f. Trauma, Burns
2) Undergoes hepatic metabolism g. Sepsis
6. Monitor Check 2 hours after dose is completed to follow improvement, if h. Alcoholism
warranted. i. Medications
i. Thiazide and loop diuretics
Magnesium (Mg2+) ii. Amphotericin
Hypermagnesemia iii. Cisplatin
1. Denition Mg > 2.4 mg/dL iv. Cyclosporine
2. Causes v. Digoxin
a. Renal insufciency 3. Signs & Symptoms
b. Iatrogenic a. Cardiac arrhythmias
3. Signs & Symptoms b. Seizure
a. Asymptomatic until Mg > 4.0 mg/dL c. Coma
b. Moderate Mg 4-12.5 mg/dL d. Death
4. EKG Changes d. Acute dialysis
a. Prolonged QT interval 6. Monitor Depends on severity
b. Atrial and/or ventricular ectopy
5. Treatment Hypophosphatemia
a. Replace IV or PO; IV preferred because enteral is slowly absorbed and 1. Denition
magnesium containing products can promote diarrhea a. Mild: < 2.7 mg/dL
b. Mild to moderate can be treated with 1-4 g of IV magnesium sulfate or 8-32 b. Severe: < 1.5 mg/dL
mEq of magnesium 2. Causes
c. Severe hypomagnesemia usually requires 4-6 g (32-48 mEq) a. Malnutrition
d. If symptomatic, start with 1-2 g (8-16 mEq) over 10 minutes b. Alcoholism
e. Decrease dose if renal function reduced by > 50% c. Alkalosis
6. Monitor Check Serum levels as needed; may be falsely elevated due to d. Diabetic ketoacidosis
magnesiums slow distribution into body tissues
e. Gastrointestinal losses
7. Magnesium as Treatment
f. Renal replacement therapy
a. Severe preeclampsia or eclampsia
g. TPN
i. Loading dose 4-6 gm IV
h. Medications
ii. Continuous infusion 1-3 gm/hr
i. Diuretics
b. Torsade de pointes
ii. Antacids
i. Loading dose 1-2 gm IV over 30-60 seconds; repeat q 5-15 minutes as needed
iii. Sucralfate
ii. Continuous infusion 0.51 g/hr
iv. Amphotericin B
c. Tolerate serum levels as high as 6-9 mg/dL as long as patient is asymptomatic
v. Corticosteroids
3. Signs & Symptoms
Phosphorus (PO42-) a. Impaired diaphragmatic contractility - hypoventilation
Hyperphosphatemia b. Acute respiratory failure
1. Denition: > 4.5 mg/dL c. Impaired myocardial contractility
2. Causes d. Weakness proximal extremities
a. Renal insufciency e. Paresthesias
b. Excessive administration f. Seizure
c. Acidosis g. Platelet dysfunction
d. Hemolysis 4. EKG Changes none
e. Rhabdomyolysis 5. Treatment
f. Tumor lysis syndrome a. Replace orally if mild and patient asymptomatic
g. Hypoparathyroidism b. If severe or symptomatic replace with IV potassium phosphate or sodium
3. Signs & Symptoms (secondary to calcium-phosphorus precipitation) phosphate
a. Crystal formation causes hypocalcemia i. Ordered in mmol
b. Crystals deposit into soft tissues causing organ damage ii. One mmol phos = 31 mg phos
c. Nephrocalcinosis 6. Monitor recheck 2 to 4 hours after infusion complete
d. Hypotension
e. Impending CV collapse
4. EKG Changes none
5. Treatment
a. Patients on renal replacement therapy need to decrease PO phosphorus in diet
b. Phosphate binders reduce absorption from the GI tract
c. Monitor feeding formulas to adjust phosphorus content

1. Bartel B and Gau E: Fluid and Electrolyte Management, Critical Care Pharmacothera- Questions
peutics. Edited by Johnson TJ. Burlington, Jones & Barlett Learning Publishers, 2012,
pp 125-50 30.1 All of the following are common causes of hypokalemia EXCEPT:
2. Gabrielli A, Layon J, Yu M: Fluids and Electrolytes, Civetta, Taylor, & Kirbys Manual A. Loop diuretic use
of Critical Care. Philadelphia, Lippincott Williams & Wilkins Publishers, 2012, pp 93-102 B. Hyper-secretion of mineralocorticoids
3. Kaplan LJ, Kellum JA: Fluids, pH, ions, and electrolytes. Curr Opin Crit Care 2010; C. Hypoaldosteronism
16: 323-31 D. Excessive vomiting, diarrhea or other GI losses
4. Kraft MD, Btaiche IF, Sacks GS, Kudsk KA: Treatment of Electrolytes Disorders in
Adult Patients in the Intensive Care Unit. Am J Health Syst Pharm 2005; 62: 1663-82
5. Lee JW: Fluid and Electrolyte Disturbances in Critically Ill Patients. Electrolyte Blood 30.2 Select the best set of parameters for Cerebral Salt Wasting, which would help differenti-
Press 2010; 8: 72-81 ate it from SIADH:
6. Sabatine MS: Pocket Medicine, 5th edition. Philadelphia, Lippincott Williams & A. Hyponatremia + Euvolemia + Urine Na+>>40mEq/L + polyuria
Wilkins Publishers, 2013 B. Hyponatremia + Hypovolemia + Urine Na+>>40mEq/L + polyuria
C. Hyponatremia + Hypovolemia + Serum Osm < 270mOsm/kg + oliguria
D. Hypernatremia + Hypovolemia + Serum Osm > 285mOsm/kg + polyuria

30.3 Which of the following are considered sequelae of hypophosphatemia?

A. Metabolic encephalopathy secondary to ATP depletion
B. Paralytic ileus
C. Rhabdomyolysis and Hemolysis
D. Impaired myocardial contractility
E. All of the above

30.4 The appropriate initial therapy for this tracing is:

A. 1-2 g calcium chloride

B. 50 mEq sodium bicarbonate
C. Synchronized cardioversion
D. 1-2 g magnesium sulfate

30.5 All of the following are associated with hypercalcemia EXCEPT:

A. Autoimmune Hypoparathyroidism
B. Primary Hyperparathyroidism
C. Sarcoidosis
D. Multiple Myeloma
E. Milk-Alkali Syndrome

31. Fluid Management in the ICU
Luke Parr MD and Aaron Joffe DO

Key Points A 55 year-old, 130-kg man with poorly controlled diabetes is admitted to
the ICU with severe redness, pain, and swelling of his right leg.
In the average 70-kg man, 60% of the bodys
T (C) 38.6
weight is water. HR (bpm) 128
RR (bpm) 24
Human albumin should not be routinely BP (mmHg) 74/53
administered and synthetic colloids (HES, Saturation 98%
dextrans, gelatin) should not be administered
to patients with sepsis. WBC (x109/L) 22
Hg (g/dL) 9.0
The Surviving Sepsis Guidelines and ATLS Na+ (mEq/L) 140
guidelines provide recommendations for fluid K+ (mEq/L) 4.2
management in severe sepsis/septic shock and Creatinine (mg/dL) 2.0
traumatic hemorrhagic shock, respectively.
Lactate (mg/dL) 6.8

Wheres the water?

Paramount to understanding uid man-
agement is an appreciation of the various
compartments into which the total body
water (TBW) is distributed (Figure 31.1).
TBW is related to the amount of lean
body mass as fat is relatively anhydrous.
Thus, men and women are considered to
be approximately 60% and 50% water,
respectively. The third space refers to
body compartments that do not readily
communicate with the vasculature such
as peritoneal, pleural, or synovial cavi-
ties. Third spacing may occur in cases of
insults such as surgery, trauma and infec-
tion. Although rarely termed this way, the
intracellular and extracellular compart-
ments represent the rst and second Figure 31.1 Proportions of Total Body Water. In the average 70kg
spaces. man, TBW = 42 kg, ICW = 28 kg, ECW = 14 kg, Interstitial = 10.5 kg
and Plasma = 3.5kg
in Table 31.1
What drives water movement between compartments?
Osmolality describes the number of osmoles per kilogram of solvent; osmolarity is the Blood components are typically prepared as fractionated components rather than whole
number of osmoles per liter of solution. Since the human body is comprised of mainly blood. One unit of packed red blood cells is about 250 ml in volume with a hemato-
water, there is little difference between the two. For practical purposes, osmolality is crit of 70%. Fresh frozen plasma and platelets can be transfused contemporaneously
easier to measure than osmolarity and is the laboratory value reported. Normal serum in an attempt to approximate transfusion of whole blood. Denitive data regarding the
osmolality is 285-295 mOsm/kg. It can be estimated by the formula: optimal ratio of plasma to red cell transfusion during massive hemorrhage is currently
(Na+ [mEq/L] X 2) + (glucose [mg/dL] / 18) + (BUN [mg/dL] / 2.3). lacking.
Although the equation is estimating serum osmolality, one should keep in mind that this
formula does combine both principles of osmolarity and osmolality (the use of 18 for How do you assess the need for uid?
glucose and 2.3 BUN converts to the values to mOsm/kg). Tonicity refers to effective Clinical assessment of the state of the extracellular uid compartment is challenging.
osmoles which result in solute-free water moving across two compartments divided by Detection of hypovolemia without shock is difcult even for the most seasoned physi-
a semi-permeable membrane. Net transcapillary uid ux is determined mainly by the cian as the history and physical exam provide limited information.2 Profound changes
hydrostatic pressure gradient between the capillary lumen and the subendothelial space. in orthostatic vital signs may be helpful in the absence of confounding medications.
Colloid osmotic pressure differences between the same two spaces have minimal impact Additionally, in the absence of ongoing uid losses, a lack of peripheral or pulmonary
on uid exchange over a wide variety of physiologic conditions.1 edema with an expanded third space makes a low circulating blood volume likely.3 Se-
rum chemistries assaying acid-base status, renal function, or urine electrolyte concentra-
What uids do you administer? tions may also be useful.
Fluid options for administration include crystalloids, colloids, and blood products.
Crystalloid solutions are the most commonly administered IV uids. They include The optimal type of resuscitation uid remains undetermined. Balanced electrolyte
normal saline (NS), balanced electrolyte solutions such as Plasmalyte-A and Ringers solutions may be associated with less renal injury than 0.9% sodium chloride solutions.
Lactate (LR) and dextrose containing solutions. Colloids are preparations of insoluble Synthetic colloids have not been shown to improve outcomes and may be detrimental
molecules dispersed throughout a water-based diluent. The perceived benet to colloids in critically ill patients. When a colloid solution is indicated, human albumin, rather
is that they are more likely to stay intravascular. The general rule of thumb that three than a synthetic colloid should be used. All colloids are contraindicated in patients with
times as much crystalloid as colloid is required for equal intravascular volume expan- traumatic brain injury.
sion has been shown to be false and is more on the order of less than 1.6:1. Colloids are
considered natural (albumin) or synthetic (gelatins, hydroxyethyl starches, and dex- Critically ill patients are often anemic. With the exception of acute anemia resulting
trans). The relative components of a number of commonly used solutions are presented from active bleeding or hemorrhage, the transfusion threshold can be safely set at 7 g/
dL with a post-transfusion goal of 7-9 g/dL.4,5,6

Table 31.1 Composition of commonly used crystalloids and colloids How do you diagnose and treat shock?
Na+ K+ Cl- Osmolality Shock is dened as a state of inadequate oxygen delivery to support aerobic
Solution (mEq/L) (mEq/L) (mEq/L) Other Ions (mMol/L) pH metabolism. General signs of shock include hypotension, tachycardia and
low urine output. The presence of a metabolic acidosis, hyperlactatemia,
Normal Saline 154 0 154 308 4.5-7.0 base decit, or low mixed venous/central venous oxygenation saturation are
(0.9% NaCl)
further clues. A directed bedside assessment can be used to broadly catego-
Lactated Ringers 130 4 109 lactate, calcium 273 6.0-7.5 rize shock states as shown in Table 31.2.
Plasmalyte 140 5 98 magnesium, 294 6.5-7.6
acetate, Hypovolemic shock can occur from a variety of causes and includes hemor-
gluconate rhage, profound diarrhea, and severe dehydration. Regardless of etiology.
D5W 0 0 0 dextrose 278 5.0 correction of hypovolemic shock includes rapid replacement of intravascular
volume until hemodynamic goals of resuscitation are met.
Albumin 5% 145 0 145 300 6.9
Albumin 25% 145 0 145 1500 6.9 A highly effective protocol for management of hemorrhagic shock in a
HES 130/0.4 154 0 154 308 4.0-5.5 trauma patient has been developed and is clearly presented in the Advanced
(Voluven) Trauma Life Support (ATLS) Guidelines. The guidelines provide recom-
mendations for the initial stabilization and evaluation of the trauma patient.
HES 450/0.7 154 0 154 309 5.9 Primary uid management includes the insertion of 2 large bore (16 gauge or
larger) intravenous catheters in a peripheral vein or a 9 French central venous

catheter, control of bleeding, and a 2 liter uid challenge. Transient and non-
responders need blood products for volume and to control coagulopathy. An Table 31.2 Findings differentiating the 4 classic categories of shock
FFP/PRBC ratio greater than or equal to 1:1.5 is associated with lower mortal- Mean RAP Mean LAP Stroke Volume SVR Mixed
ity. Ultimately, source control is the most important intervention in traumatic Type (neck veins) (lungs) (pulse volume) (skin) Venous O2
hemorrhagic shock.7
Hypovolemic , at , clear , cool/mottled

Cardiogenic shock is caused by the hearts inability to pump effectively, Cardiogenic , rales , cool/mottled
whether due to intrinsic myocardial disease, arrhythmia or valvular disease. Distributive , at , clear , warm/
Diastolic heart failure is usually a compliance problem, whereas systolic heart diaphoretic
failure is primarily a failure of the heart to pump. Management of cardiogenic
Obstructive* , clear , cool/mottled
shock often involves manipulating preload (diuresis and/or nitrates), afterload
(vasopressors, ACE inhibitors, intra-aortic balloon pump), and/or contractility *Classic ndings of a massive pulmonary embolism. Findings vary if the etiology is tension
(inotropes). Pulmonary artery catheters have historically been used to help cli- pneumothorax or cardiac tamponade.
nicians in the management of cardiogenic shock but its use has not been shown
to improve survival.

Distributive shock is due to loss of vascular tone and/or increase in vascular permeabili- This patient has septic shock. Hemodynamic resuscitation
ty leading to hypotension and tissue hypoperfusion. Specic etiologies may include sep-
sis, anaphylaxis, fulminant hepatic failure, and endocrine dysfunction such as adrenal goals as described by the Surviving Sepsis Campaign
crisis or thyroid storm. Neurogenic shock is related to a loss of sympathetic tone from guidelines should be targeted. Hypotension and tachycardia
the spinal cord leading to accid vasculature, often with bradycardia, and is best treated have further resulted in demand ischemia. Other etiologies
with uids, vasopressors, and inotropes. Septic shock is by far the most common form of his shock including hemorrhagic and pulmonary embolism
of distributive shock. are less likely.

The Surviving Sepsis campaign recommends initial resuscitation targets of a CVP 8-12 Fluid resuscitation with an initial bolus of 20-30 mL/kg is
mmHg, MAP 65 mmHg, UO 0.5 ml/kg/h, and central venous oxygen saturation appropriate. Central access should be considered. A urinary
greater than 70% for patients in severe sepsis and septic shock. Crystalloids are the catheter and arterial line should be placed. If the initial uid
uid of choice with an initial challenge of at least 2 liters or 30 mL/Kg. Albumin may bolus does not resolve his hypotension and tachycardia, a
have a role only after substantial amounts of crystalloids are given. Synthetic colloids vasopressor should be started to maintain his mean arterial
are contraindicated in these patients. Barring other indications for transfusion, a goal pressure greater than 65 mmHg. Although his hemoglobin
hemoglobin of 7-9 g/dL is adequate and FFP is not indicated, except in the presence of is greater than 7 g/dL, a packed red cell transfusion may be
bleeding or planned procedures.8 appropriate, but only after other hemodynamic goals have
been reached. Aggressive resuscitation, in conjunction with
Obstructive shock, which can be conceptualized as intra- or extra- cardiac obstruction treatment of the infection, gives this patient his best chance
to either inow or outow, may result from cardiac tamponade, tension pneumothorax, at survival and optimal recovery.
pulmonary embolism, or severe aortic stenosis. Administration of uid is merely a
temporizing measure, as correction of obstructive shock requires rapid correction of the
underlying problem.

1. Woodcock TE and Woodcock TM: Revised Starling equation and the glycocalyx model Questions
of transvascular uid exchange: an improved paradigm for prescribing intravenous uid
therapy. Br J Anaesth 2012; 108(3):384-94. 31.1 The use of colloid solutions in uid management is preferred in which of the following
2. McGee S, Abernethy WB 3rd, Simel DL: The rational clinical examination. Is this patients?
patient hypovolemic? JAMA 1999; 281(11):1022-9. A. Acute traumatic brain injury
3. Stphan F, Flahault A, Dieudonn N, Hollande J, Paillard F, Bonnet F: Clinical evalu- B. Acute pancreatitis
ation of circulating blood volume in critically ill patients--contribution of a clinical scoring C. Septic shock
system. Br J Anaesth 2001; 86(6):754-62. D. None of the above
4. Hbert PC, Wells G, Blajchman MA, Marshall J, Martin C, Pagliarello G, Tweeddale M,
Schweitzer I, Yetisir E, and the Transfusion Requirements in Critical Care Investigators:
A multicenter, randomized, controlled clinical trial of transfusion requirements in critical 31.2 An elevated central mixed-venous oxygen saturation is classically found in which of the
care. N Engl J Med 1999; 340(6):409-17. following conditions?
5. Carson JL, Terrin ML, Noveck H, Sanders DW, Chaitman BR, Rhoads GG, Nemo G, A. Hemorrhagic shock
Dragert K, Beaupre L, Hildebrand K, Macaulay W, Lewis C, Cook DR, Dobbin G, Zakriya B. Septic shock
K, Apple F, Horney R, Magaziner J:. Liberal of Restrictive Transfusion in High-Risk Pa- C. Cardiogenic shock
tients after Hip Surgery N Engl J Med 2011; 365(26):2453-62. D. Massive pulmonary embolism
6. Villanueva C, Colomo A, Bosch A, Concepcion M, Hernandez-Gea V, Aracil C, Grau-
pera I, Poca M, Alvarez-Urturi C, Gordillo J, Guarner-Argente C, Santalo M, Muniz E, 31.3 Which of the following is the best indicator of hypovolemia
Guarner C: Transfusion Strategies for Acute Upper Gastrointestinal Bleeding. N Engl J A. Gastric tonometry
Med 2013; 368(1):11-21. B. Pulse pressure variation
7. Committee on Trauma, American College of Surgeons (2008). ATLS: Advanced Trauma C. Stroke volume variation
Life Support Program for Doctors (8th ed.). Chicago: American College of Surgeons. D. Orthostatic vital signs
8. Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal S, Sevransky J, Sprung
C, Douglas I, Jaeschke R, Osborn T, Nunnally M, Townsend S, Reinhart K, Kleinpell R,
Angus D, Deutschman C, Machado F, Rubenfeld G, Webb S, Beale R, Vincent JL, Moreno
R and the Surviving Sepsis Campaign Guidelines Committee: Surviving Sepsis Campaign:
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Crit
Care Med 2013; 41(2):580-637.

32. Renal Replacement Therapy
Matthew J F Sigakis MD and Edward A Bittner MD PhD

Key Points A 72 year-old man is admitted to the ICU after open repair of a thoraco-
abdominal aortic aneurysm. His postoperative course is complicated
Renal Replacement Therapy (RRT) is a
by acute kidney injury, respiratory failure and hypotension. On post-
operative day (POD) # 3, renal replacement therapy is initiated via
common therapy provided in the ICU. continuous veno-venous hemodialysis. After 1 week, there is improvement
in his hemodynamics and he is transitioned to conventional intermittent
RRT can be performed continuously (CRRT) hemodialysis. He is transferred to the oor on POD#9.
or intermittently (IHD); one has not been
demonstrated to be superior over the other.

Although CRRT is preferred in

hemodynamically unstable patients, the final
modality will depend on physician preference
and hospital resources.

3 major principles in RRT are ultrafiltration,

diffusion, and convection.
Acute kidney injury (AKI) in the Intensive Care Unit (ICU) is common and can range from mild elevation in
creatinine to anuric renal failure. Once a patient has developed severe AKI, the therapeutic options are limited
with the mainstay of treatment being renal replacement therapy (RRT).

Indications for RRT

There is a paucity of evidence to guide the optimal time to initiate RRT. In most instances, the decision to ini-
tiate RRT is based on development of life threatening conditions (Table 32.1). There is no generally accepted
azotemia threshold for RRT initiation. Once a decision to commence RRT is made, the components of the
prescription include the modality, anticoagulation, and intensity of treatment.

Principles of RRT
RRTs are classied by the transport process used to remove solutes and toxins from the blood. All forms of
RRT rely on the principle of allowing water and solute movement through a semipermeable membrane and
then discarding the waste products, normally down the drain.

Ultraltration is the process by which the movement of water occurs across a semipermeable membrane due
lithium, urea) and uid.
Table 32.1 Indications for RRT
Primary Secondary Hemoltration
Alcohol and drug intoxications Endotoxic shock Blood is pumped through an extracorporeal system that incorporates a semi-permeable
membrane. The hydrostatic pressure that is created on the blood-side of the membrane
Fluid management for oliguria/anuria Acute hepatic failure drives plasma across the membrane (ultraltration). Molecules that are small enough
Hyperkalemia Plasmapheresis (in lieu of) to pass through the membrane (typically <50,000 Daltons) are dragged across the
membrane with the water by the process of convection. The ltered uid (ultraltrate)
Hypothermia Severe dysnatremia is discarded and a replacement uid is added in an adjustable (in volume and composi-
Metabolic acidosis (pH < 7.1) Severe rhabdomyolysis tion) fashion. Hemoltration is typically used for moderate to large molecules (5,000 to
50,000 Daltons) such as cytokines and compliment.
Rapidly climbing urea/creatinine
Refractory uid overload Hemodialtration
Uremia with acute signs of pericarditis, neu- A combination of dialysis and ultraltration, it has the benets of both techniques but to
ropathy, mental status changes or refractory a lesser extent than when the individual techniques are used on their own.
Slow continuous ultraltration
to a trans-membrane pressure gradient. Used when the only requirement is water removal. It can remove up to 6 liters of uid
in a day. Solute removal is minimal.
Diffusion and convection are two processes by which solutes move across a semiperme-
able membrane (Figure 32.1).3 Diffusion is the movement of solutes from an area of
higher solute concentration to an area of lower solute concentration across a semiperme-
able membrane. Convection occurs when the trans-membrane pressure gradient drives
water across a semipermeable membrane (ultraltration) and drags solutes with it. In
this process, membrane pore diameter limits the size of the solutes that can pass though

Modalities of RRT
RRT modalities include intermittent hemodialysis, continuous renal replacement thera-
py, peritoneal dialysis and newer hybrid therapies, such as extended duration dialysis
or sustained low-efciency dialysis.

The distinguishing characteristics of these modalities include the uid transport process
(hemodialysis vs. hemoltration), duration (intermittent vs. continuous) and membrane

Fluid Transport Process (Figure 32.2)

Blood is pumped through an extracorporeal system where it is physically separated
from a crystalloid solution (dialysate) by a semi-permeable membrane. Solutes move
across the membrane along their concentration gradient from one compartment to the
other by Fick`s laws of diffusion. For example, bicarbonate moves from dialysate
to blood (higher concentration in dialysate) whereas urea and potassium move from
blood to dialysate (lower concentration in dialysate). In order to maintain concentra-
tion gradients and, therefore, enhance the efciency of the system, the dialysate ows
counter-current to the ow of blood (i.e., they ow in opposite directions of each other).
When removal of water is required, the pressure on the blood-side of the membrane is Figure 32.1 Transport of solutes across a semipermeable membrane by convection
increased to force water molecules to pass into the dialysate. Hemodialysis is typi- and diffusion. [Adapted from Tolwani, et al]
cally chosen for removal of small molecules < 500 Daltons and electrolytes (potassium,
Sustained Low-Efciency Dialysis (SLED) and Extended Day Dialysis (EDD)
SLED and EDD are dialytic modalities that use conventional hemodialysis machines.
These machines are able to provide slower blood and dialysate ows. They com-
bine the advantages of CVVH and IHD to allow for improved hemodynamic stability
through gradual solute and volume removal as in CRRT while providing high solute
clearances as in IHD. These treatments can be performed intermittently based on the
needs of the patient and do not need to be interrupted for various beside diagnostic and
therapeutic procedures that may be required in critically ill patients.

Membrane permeability
Low ux (Cellulose based)
Low permeability to water and is typically used for hemodialysis.

High ux (Synthetic)
High permeability to water and is typically used for hemoltration.

Other forms of RRT

Peritoneal Dialysis (PD)
Dialysate is placed into a patients abdomen where the peritoneum is used as a mem-
brane across which uids and solutes (electrolytes, urea, glucose, albumin and other
small molecules) are exchanged from the blood. The dialysate is removed and replaced
periodically. High volume and continuous PD does exist. It is rarely used in the ICU to
Figure 32.2 Components of continuous veno-venous hemodialysis (CVVHD); central treat AKI.
double-lumen veno-venous catheter (CDL-VVC), an extracorporeal circuit and hemol-
ter, blood pump, efuent and dialysate. [Adapted from Tolwani, et al.] Arterio-venous RRT
Used to treat AKI via temporary central arterial (outow) and venous (inow) catheters.
Duration Arterio-venous RRT is associated with greater vascular morbidity than veno-venous ac-
Intermittent Hemodialysis (IHD) cess and depends on an adequate arterial blood pressure to drive blood ow. As a result,
it has largely been replaced by veno-venous RRT.
Traditionally, severe AKI has been managed with IHD that is empirically delivered
over 3-5 hours per session, 3-6 sessions per week. Decisions regarding dialysis session
duration and frequency are based on patient metabolic control, volume status, and pres- Arterio-venous stula or graft
ence of hemodynamic instability. A major advantage of IHD is rapid solute and volume Surgically created communication between the native artery and vein in an extremity,
removal. In addition, IHD usually has a decreased need for anticoagulation compared allowing blood to bypass capillaries and ow more freely. A 14-gauge needle is in-
with other types of RRT because of the faster blood ow rate and shorter duration of serted in the vein or graft in a location that is proximal to the artery. This access diverts
therapy. The main disadvantage of IHD is the risk of hypotension resulting from rapid blood to the dialysis machine. A second 14-gauge needle is inserted in the vein or graft
electrolyte and uid removal. Rapid solute removal from the intravascular space can in a location that is distal to the artery that allows dialyzed blood to return to the patient
result in cerebral edema limiting this modality for patients with head trauma or hepatic (Figure 32.3). A patent graft typically has a palpable or auscultatory thrill. An arterio-
encephalopathy. venous stula or graft cannot be used for CRRT as it is nearly impossible to the secure
the needles to prevent dislodgement.
Continuous veno-venous hemodialysis (CVVHD), hemoltration (CVVH) and hemodi-
altration (CVVHDF) Modality and Outcome
Continuous in duration with lower ow rates, there tends to be less hemodynamic dis- Studies which compare modalities have failed to demonstrate any survival advantage
turbance. In addition, solute and electrolyte removal occur over a longer period of time for continuous versus intermittent therapy. However, these studies have been limited by
resulting in less acute osmolar changes. These modalities require continuous anticoagu- issues related to study design, such as exclusion of patients with hemodynamic instabil-
lation and are more expensive to utilize than IHD. Components of CRRT include central ity, improper randomization, differences in baseline characteristics between study popu-
access with a large bore (at least 10 French) double-lumen venous catheter, an extracor- lations and high crossover rates between modalities. In the absence of data suggesting
poreal circuit with lter, a blood pump, and an efuent pump (Figure 32.2).3 benet of one over another, choosing a modality should be guided by the patients
clinical status, local medical and nursing expertise, and availability of RRT modalities.

Transitions in modality are common due to the changing needs of patients during their Currently, heparin is administered
hospital course. systemically or pre-lter, if needed.
Intermittent ushing with saline or
Technical considerations pre-lter hemodilution may be used
Access as an alternative to anticoagulation to
Central venous access via double lumen catheter (1114 Fr) prevent lter clotting.
Internal jugular or femoral vein is preferred. Short runs of dialysis (<2
hours) may be performed without
Subclavian vein is used with caution given propensity for stenosis and inability to anticoagulation.
compress in the event of hemorrhage.
Runs can be extended for
The proximal port removes blood and it is returned through the distal lumen at the patients with thrombocytopenia or
catheter tip to minimize recirculation of ltered blood. coagulation disorders.
Tunneled catheters can be placed if dialysis is to be prolonged. PD can be an alternative RRT
modality for patients with an extreme
Anticoagulation mortality/morbidity risk from
RRT can activate the clotting cascade given contact between blood and non- anticoagulation.
biological surface. RRT without anticoagulation is
Anticoagulation is typically used for both intermittent and continuous forms of RRT. common in patients with coagulation
Most common anticoagulant is unfractionated heparin; citrate is a common second- abnormalities.
choice agent (see below). Regional heparin/protamine
Other approaches exist to minimize clotting within the extracorporeal circuit and can anticoagulation:
be utilized when there is increased risk of bleeding (see below). No longer recommended. Protamine
administration can result in a Figure 32.3 Typical access for chronic hemo-
Table 32.2 Drugs cleared by RRT
number of severe side effects dialysis. [
including anaphylaxis, hypotension, File:Fistola_radiocefalica.svg, licensed under
Barbiturates Antibiotics: cardiac depression, leukopenia and Cretative Commons Attribution]
Ethylene glycol - Aminoglycosides
thrombocytopenia. There is also risk
of a rebound anticoagulant effect,
Lithium - Carbapenems due to the shorter half-life of protamine compared with heparin.
Metformin - Cephalosporins
Heparin-induced thrombocytopenia
Methanol - Metronidazole
Heparin anticoagulation is contraindicated; therefore the dialysis system must also
Salicylates - Penicillins be heparin free.
Regional citrate anticoagulation:
Resources Citrate is infused into the blood of the afferent limb, which binds to ionized calcium
CRRT is more labor intensive and more expensive than IHD. inhibiting coagulation. Citrate is removed during the dialysis process, but may
Clinician experience may be important. enter the systemic circulation leading to hypocalcemia. Intravenous calcium
supplementation is frequently required. In patients with reduced citrate metabolism,
such as in liver failure and in patients with pre-existing hypocalcemia and/or
Pharmacokinetics hypomagnesemia, extra caution is warranted.
Drugs are more readily cleared by RRT if they are water-soluble and not highly Argatroban, a direct thrombin inhibitor, is sometimes used (off label use):
protein-bound. As a patients protein level falls, the free fraction of the drug increases Argatroban is hepatically metabolized and safe in patients with intact hepatic
causing greater clearance. (See Table 32.2) function. Argatroban has a short half-life of approximately 35 minutes in patients
Drugs given between intermittent periods of dialysis will not be cleared until a with end-stage kidney disease (ESKD). Monitor with activated clotting and partial
subsequent session. thromboplastin times (NOT PT and/or INR).

Patient factors impacting RRT Hemodynamic instability

Increased risk of bleeding Several precautions must be taken including less aggressive ultraltration, longer
Anticoagulation may be needed for IHD or CRRT to prevent clotting of the lter. runs, and use of blood volume measurements to guide ultraltration.

CRRT, when available, is preferred over IHD because there is less hemodynamic Acute liver failure or acute on chronic liver failure
disturbance. AKI may be secondary to hepatorenal syndrome.
RRT may help to stabilize the hemodynamic status by correction of blood pH. Cerebral edema, increased intracranial pressure and hyponatremia may be present.
CRRT with special attention for hemodynamic stability and maintenance of cerebral
Cerebral edema or intracranial hypertension perfusion pressure is warranted.
CRRT is preferred over intermittent RRT:
There are less frequent decreases in systemic blood pressure that could lead to Complications
cerebral ischemia. In addition, there are less frequent tonicity/osmolarity changes of Vary in nature relating to the dialysis catheter, the extracorporeal circuit, and therapy,
the systemic circulation that can worsen cerebral edema. itself. (See Table 32.3)
Traumatic brain injury with risk of intracranial bleed
Consider RRT without anticoagulation.
PD is an option. However, increased abdominal pressure from dialysate may
1. Hall NA, Fox AJ: Renal replacement therapies in critical care. Br J Anaesth: Contin
translate into increased intracranial pressure. In addition, intra-abdominal Educ Anaesth Crit Care Pain 2006; 6:197-202
hypertension may decrease systemic preload and increase afterload, leading to lower 2. Palevsky PM: Indications and timing of renal replacement therapy in acute kidney
blood pressure and decreased cerebral perfusion pressure. injury. Crit Care Med 2008; 36(4 Suppl):S224-8
3. Tolwani A: Continuous Renal-Replacement Therapy for Acute Kidney Injury. N Engl J
Med 2012; 367:2505-14
Hyponatremia 4. Baker A, Green R: Renal replacement therapy in critical care, tutorial of the week 194.
World Federation of Societies of Anaesthesiologists. 2010 August 30:1-15
Chronic hyponatremia corrected rapidly may cause osmotic demyelination
Renal replacement uid with reduced sodium concentration may be used. However,
this may also decrease plasma chloride and/or bicarbonate concentrations. Frequent
monitoring of sodium, bicarbonate, and pH is warranted.

Elevated serum urea

Urea >175 mg/dl
Risk of dialysis disequilibrium syndrome, a neurological condition characterized by
nausea and headache. The mechanism is thought to be a decrease in serum osmolarity Questions
(due to decreased serum urea during dialysis), with slower equilibration of intracranial
urea concentration leading to cerebral edema. Preventative measures to maintain 32.1 The following statements about Continuous Renal Replacement Therapy (CRRT) are true,
serum osmolarity include decreasing the dose of dialysis, slowing treatment time, or A. CRRT is more cost effective than IHD
initiation of RRT with ultraltration followed by dialysis. B. CRRT is preferable to IHD in patients with acute brain injury or cerebral edema.
C. There is no known survival benet using CRRT versus IHD.
D. CRRT is preferred in patients who have an unstable cardiovascular status.

Table 32.3 Complications of RRT 32.2 The following statements regarding RRT are true, except:
A. Internal jugular or femoral vein central access is preferred over subclavian vein for
Air emboli Catheter related: dialysis catheter placement.
B. Water-soluble drugs are more easily removed by RRT than protein-bound drugs.
Altered drug kinetics - Bleeding C. Regional citrate anticoagulation can be used during RRT for patients with HIT.
D. There is an established role for RRT in the ICU for treatment of septic shock in patients
Blood loss - Infection with normal renal function.
Electrolyte imbalances - Line disconnection/malfunction
33.3 The following statements comparing dialysis with ltration are true, except:
Hemodynamic instability - Pain A. Filtration is more effective than dialysis at removing water.
B. A low ux membrane is typically used for ltration and a high ux membrane is typi-
Hypothermia - Pneumothorax cally used for dialysis.
C. Filtration in more effective than dialysis at removing cytokines and dialysis is more ef-
Platelet consumption - Thrombosis fective at removing small molecules.
Anticoagulation related: bleeding, HIT D. Filtration depends on convection and dialysis depends on diffusion.

Section 8: Hematology and Transfusion


Thromboembolic Disease

Coagulopathies in the ICU

Transfusion Therapy
33. Thromboembolic Disease
Tracy Jobin McGrane MD

Key Points A 32 year old female is admitted to the neurological intensive care unit
status post a craniectomy for resection of a frontal lobe high grade
The clinical presentation may vary from a
glioma. Three days after admission, she is tachycardic and complains of
shortness of breath. Her physical exam is otherwise unremarkable. Her
patient being asymptomatic to one in shock, chest radiograph (CXR) and arterial blood gas analysis are normal. Later
making it a challenging diagnosis if it is not that day, she develops sudden respiratory distress with hypotension and
thought of as part of the differential diagnosis. hypoxia. A helical computed tomography (CT) scan reveals a pulmonary
Diagnostic workup corresponds to the
severity of the patients clinical presentation.

Anticoagulation is the mainstay of therapy.

Hemodynamically unstable patients may

require thrombolysis or surgical embolectomy.

Venous thromboembolism (VTE) is a pathologic clot formation within the veins and can refer to either a deep
venous thrombosis (DVT) or a pulmonary embolism (PE). It is estimated that greater than one million people
in the United States are affected by a PE each year, with approximately 10-20% resulting in death, but the
true incidence is believed to be much higher based on post mortem data. The majority of preventable deaths
associated with PE are related to a missed diagnosis rather than a failure of existing therapies. Many screening
studies for venous thromboembolism (VTE) lack sensitivity and specicity. Several noninvasive diagnostic
techniques have been developed to improve the accuracy of the diagnosis; however, no single noninvasive
diagnostic test is sensitive or specic enough for the diagnosis in all patients. The cornerstone of management
involves identication of high risk groups and treatment with adequate prophylactic measures.

A. Exact incidence unknown but studies estimate more than one million cases in the US each year.
B. The majority of VTE deaths are caused by PE.
C. Initial clinical presentation is sudden death in approximately 20% of all cases.
D. Mortality of untreated PE is approximately 30%; once diagnosed and treated, mortality is 2.5%.
E. Risk Factors for VTE
1. History of VTE
2. Age > 40 yr
3. Surgery Diagnosis of VTE/PE
4. Prolonged immobility A. Clinical presentation-extremely varied ranging from asymptomatic to any of the
5. Cerebrovascular accident symptoms below
6. Congestive heart failure 1. VTElimb edema/pain, differential limb circumference, Homans sign, distended
7. Malignancy collateral veins, increased temperature if infection present
8. Trauma 2. PEdyspnea, pleuritic pain, tachypnea, tachycardia, hypoxemia, hypocarbia,
9. Obesity hemoptysis, inltrate on CXR, or sustained hypotension without an obvious cause
10. Pregnancy or recent delivery B. Clinical probability assessment
11. Estrogen therapy 1. Suspected PE based on clinical presentation and risk factors
12. Inammatory bowel disease a. Clinical judgment is heavily weighted in most diagnostic algorithms
13. Inherited or acquired defects in blood coagulation factors b. Clinical probability tools such as Wells Criteria, Geneva Score and Pulmonary
Embolism Severity Index (PESI) help stratify patients based on probability of PE
C. Diagnostic workup
1. Hemodynamically stable
A. Virchows triad: venous stasis, hypercoagulable state, and vascular endothelial
injury a. Low or intermediate clinical probability check D-Dimer (usually omitted
in hospitalized patients because specicity is reduced in this population)
B. Approximately 50% of patients with a VTE will have more than one risk factor
i. D-Dimer normal PE is ruled out
ii. D-Dimer elevated proceed with CTA to either rule out or conrm
diagnosis (if this is not available or if patient has chronic kidney disease
Prophylaxis or patient has allergy to contrast dye, ventilation-perfusion scanning is an
A. Pharmacologic agents acceptable alternative)
1. Heparins b. High clinical probabililty proceed with CTA
a. Unfractionated heparin-monitoring not needed for prophylaxis 2. Hemodynamically unstable
b. Low molecular weight heparin (LMWH)-monitoring: not needed a. If safe to transport, proceed with CTA, if available, or echocardiography if
i. Recent meta-analysis has shown LMWH to be superior to unfractionated CTA not available
heparin in preventing PE. b. If patient unsafe to transport and high clinical probability, proceed with
c. Complications transthoracic or transesophageal echocardiography to evaluate for right
i. Bleeding ventricular (RV) dysfunction to either rule out or conrm diagnosis of PE
ii. Thrombocytopeniasecondary to immune IgG-mediated response; may lead i. rarely a thrombus can be seen within the pulmonary arteries or RV
to arterial thrombosis D. Diagnostic options
iii. Resistance to heparinantithrombin III deciency 1. Pulmonary angiographyconsidered the gold standard but is rarely performed
iv. Osteoporosisoccurs in approximately 30% treated with long-term today
unfractionated heparin therapy a. Requires expertise in performance and interpretation, is invasive, and has
2. Vitamin K antagonist associated risks
a. Warfarin b. Usually reserved for patients with chronic thromboembolic pulmonary
b. Complications
c. Comparable outcome results between pulmonary angiography and CTA of
i. Bleeding approximately 1% VTE rate within 6 months
ii. Skin necrosisin patients with protein C or S deciency 2. Contrast enhanced helical CT scan
B. Mechanical agents a. Reported sensitivity ranges from 57-100% and its specicity ranges from 78-
1. Early ambulation, leg elevation, physiotherapy 100%
2. Graduated compression stockings b. Sensitivity and specicity vary with the location of the emboli, ranging from
3. Intermittent pneumatic compression 90% for emboli involving the main and lobar pulmonary arteries to much lower
4. Prophylactic IVC lterif anticoagulation contraindicated or patient has VTE rates for segmental and subsegmental pulmonary vessels
recurrence despite adequate anticoagulation c. A normal CT scan may indicate a substantially reduced likelihood of
embolism but negative predictive value is lower than with a negative V/Q scan
3. Ventilation perfusion (V/Q) scan
a. Previously had a central role in the diagnosis of embolism; can be a valuable i. Released from cardiac ventricular cells in response to high ventricular lling
tool when CTA contraindicated and the results are denitive pressures; is an indicator of myocardial wall stress and hypoxia
b. A normal scan rules out the diagnosis of embolism, and a high probability one ii. In one series, serum BNP was elevated in 80% of patients with acute PE
is strongly suggestive of embolism and signicant RV overload
c. Large trials have demonstrated that most patients with suspected PE who E. Diagnosis of DVT
undergo V/Q scan do not have ndings that are considered denitive 1. Contrast venography
d. High clinical suspicion and high probability lung scan: PE in 96% a. The reference standard for the diagnosis of VTE
e. Low clinical suspicion and low probability lung scan: PE in 4% b. Noninvasive tests have supplanted the venogram
f. Patients must have a normal chest xray and normal ventilation patterns for this 2. Impedance plethysmography (IPG)
exam. a. Overall sensitivity and specicity of 83% and 92% respectively
4. Echocardiography b. False positive results with tensing of the leg muscles, reduces arterial ow
a. Massive PE is associated with right ventricle (RV) enlargement, RV free and compression by an extravascular mass
wall hypokinesis with preservation of apical contractility, dilation of pulmonary 3. Ultrasonography with color Doppler ow (duplex scan)
arteries, and elevated RV pressure.
a. Sensitivity for DVT is 97%; specicity is 99%
b. According to the International Cooperative Pulmonary Embolism Registry,
RV hypokinesis predicted an increased risk of death within 30 days in patients b. Does not identify deep pelvic DVT
with SBP > 90 mm Hg. 30 day survival rates in patients with or without RV c. Cannot distinguish between occlusion from external pressure vs. thrombosis
hypokinesis were 84% and 91% respectively. d. Less sensitive in identifying asymptomatic, isolated calf vein and recurrent
5. Magnetic Resonance Angiography/Venography (MRA/MRV) thrombosis
a. Shown to have insufcient sensitivity and a high rate of technically e. Predicted value is greater than that of IPG
inadequate images when used for diagnosing PE (PIOPED III)
6. Review of other diagnostic workup Treatment
a. Electrocardiogram A. Local measureselevation of extremity, warm compresses; to be used as adjunct to
i. The classic S1Q3T3 pattern (deep S-wave in lead I, Q-wave in lead III, and other measures
inverted T-wave in lead III) suggests right heart strain and should prompt B. Anticoagulation (should begin before diagnostic studies if PE is intermediate or
consideration for PE work up high probability)
ii. Neither sensitive nor specic for PE; this pattern is only seen in a small 1. Unfractionated heparin infusion-adjusted dose
percentage (approximately 10%) of patients with a PE a. Adjust to keep PTT 1.5 - 2.0 times control
b. ABG b. Follow with warfarin within 24 hours; continue warfarin for at least 3 months
i. Previous studies have shown that a PE cannot be excluded with a normal 2. LMWHxed dose, subcutaneous (SC) regimens proven as effective treatment
alveolar-arterial gradient for VTE and PE, usually not monitored
c. CXR 3. Direct thrombin inhibitors-adjusted dose
i. May see ipsilateral elevation of the diaphragm on affected side, wedge- a. Does not require antithrombin III cofactor
shaped inltrate, focal oligemia, or an enlarged right descending pulmonary b. Used mainly for patients with heparin induced thrombocytopenia
artery but these are neither sensitive nor specic
c. Can have unpredictable anticoagulation, need for intensive lab monitoring,
d. D-dimer and potential drug-drug interactions
i. Endogenous marker for brinolysis C. Thrombolytic therapy
ii. Highly sensitive but nonspecic screening test for suspected VTE 1. Considered in patients deteriorating despite aggressive medical therapy; and
iii. Elevated levels present in nearly all patients with VTE but can also be normotensive patients with evidence of RV impairment.
elevated with advance aged, pregnancy, trauma, recent surgery, inammation, 2. Agents: Streptokinase; Urokinase; Alteplase.
and cancer
D. Pulmonary embolectomy
e. Troponin
1. For hemodynamically unstable patients with PE and in whom thrombolysis is
i. Elevated level not specic for PE contraindicated
ii. Elevated level in presence of PE correlates with worse RV function 2. Historically accompanied by a high mortality rate (up to 30%)
iii. Normal level has a 97-100% negative predictive value for in-hospital E. Inferior Vena Cava lter (IVC)
1. For patients who have contraindications to anticoagulant therapy or an inability
f. Brain Natriuretic Peptide (BNP) to be adequately anticoagulated
2. Higher long term incidence of DVT but lower risk of PE
3. Retrievable IVC lter should be considered and removed as soon as possible to Questions
avoid endothelialization
33.1 A 76-year-old man is 5 days post intracranial hemorrhage and develops dyspnea with
pleuritic chest pain. Vitals: T = 38.6C, BP - 82/48, P = 125. CXR and ECG are unrevealing. ABG
on room air shows: pH = 7.48, PaCO2 = 32, PaO2 = 72. What should be the next step?
CONCLUSIONS and RECOMMENDATIONS A. Intravenous heparin and no further diagnostic testing.
B. Intravenous heparin followed by thrombectomy.
VTE can be difcult to diagnosis due to its varied clinical presentation. Suspected PE C. Echocardiogram followed by possible embolectomy.
in the stable critically ill patient should receive a CTA, unless contraindicated. If patient D. CTA followed by intravenous heparin.
is unstable, consider urgent echocardiogram to rule out right ventricular strain or antico- E. Pulmonary arteriography.
agulate until stable enough for diagnosis to be obtained. Consider thrombolytic therapy
in patients with PE and rapid deterioration or pulmonary embolectomy for unstable 33.2 A 58-year-old woman with renal failure develops acute dyspnea 7 days after hip replace-
ment surgery. She has a history of 90 pack-years of smoking, and has received heparin, 5000
patients in whom thrombolysis is contraindicated. IU SQ Q12 hrs since her admission. Which one of these measures is most appropriate at this
A. Discontinue heparin, as the dyspnea may be a complication of therapy.
B. Obtain a pulmonary arteriogram, because a V/Q scan is unreliable in heavy smokers.
REFERENCES: C. Obtain a V/Q scan, then anticoagulate if scan is high probability.
1. Agnelli G and Becattini C: Acute Pulmonary Embolism. N Engl J Med 2010; 363:266- D. Anticoagulate with IV heparin (PTT 1.5 normal), then start warfarin in 5 to 7 days.
74. E. Obtain a CTA, then anticoagulate if scan is high probability.
2. Fedullo PF and Tapson VF: The Evaluation of Suspected Pulmonary Embolism. N Engl
J Med 2003; 349:1247-56. 33.3 Which one of the following statements is true about the initial presentation/diagnosis of
3. Hunt JM and Bull TM: Clinical Review of Pulmonary Embolism: Diagnosis, Prognosis, acute PE?
and Treatment. Med Clin North Am 2011; 95:1203-22. A. Normal ndings on ABG exclude the possibility of PE.
4. Alhazzani W, Lim W, Jaeschke RZ, Murad MH, Cade J and Cook DJ: Heparin Throm- B. Absence of elevated hemidiaphragm on CXR excludes possibility of PE.
boprophylaxis in Medical-Surgical Critically Ill Patients: A Systematic Review and Meta- C. CTA is considered the gold standard for diagnostic testing of PE.
Analysis of Randomized Trials. Crit Care Med 2013; 41(9):2088-98. D. Hormone replacement therapy in postmenopausal women is a risk factor for venous
5. Park B, Messina L, Dargon P, et al: Recent Trends in Clinical Outcomes and Resource thromboembolism.
Utilization for Pulmonary Embolism in the United States: Findings from the Nationwide E. Patients with clinically signicant PE have characteristic manifestations that suggest its
Inpatient Sample. Chest 2009; 136:983-90. presence.
6. Spencer FA, Emery C, Lessard D, et al: The Worcester Venous Thromboembolism
Study: A Population-Based Study of the Clinical Epidemiology of Venous Thromboembo-
lism. J Gen Intern Med 2006; 21:722-7.
7. Becattini C, Vedovati MC, Agnelli G: Prognostic Value of Troponins in Acute Pulmo-
nary Embolism: A Meta-Analysis. Circulation 2007; 116:427-33.
8. Stein PD, Goldhaber SZ, Henry JW, et al: Arterial Blood Gas Analysis in the Assess-
ment of Suspected Acute Pulmonary Embolism. Chest 1996; 109:78-81.
9. Stein PD, Chenevert TL, Fowler SE, et al: Gadolinium-enhanced Magnetic Resonance
Angiography for Pulmonary Embolism: A Multicenter Prospective Study (PIOPED III). Ann
Intern Med 2010; 152:434-43.
10. Guyatt GH et al: Executive Summary: Antithrombotic Therapy and Prevention of
Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Prac-
tice Guidelines. Chest 2012; 141 (suppl 2): 7S-47S.

34. Coagulopathies in the ICU
Nicholas Pesa MD and John Klick MD

Key Points A 72 year-old man is taken emergently to the OR from the cath lab in
cardiogenic shock. He had received ticagrelor, an allosteric ADP receptor
Coagulation is an incredibly complex and
antagonist, in the cath lab and angiography revealed severe triple vessel
disease including a 95% left main coronary artery occlusion, at which
elegant system that must be understood point he was rushed to the OR. After CABG while attempting to wean
well in order to recognize and treat the off cardiopulmonary bypass, severe right ventricular dysfunction was
coagulopathic ICU patient. encountered, prompting a return to CPB and placement of an Abiomed
right ventricular assist device. He received 8 units of PRBC in the OR, as
There are numerous causes of hyper- and well as 5 units of FFP, 2 units of platelets, and 2 units of cryoprecipitate.
hypocoagulability that can overlap and coexist He is on multiple inotropic and vasopressor agents. His rst hour in the
in the ICU patient. ICU he has over 300 cc of sanguineous output from the chest tubes. His
rst hematocrit is 19 in the ICU.
Antithrombotic agents are useful
pharmacological agents in the ICU patient but
must be understood well for safe use.

Pharmacological agents promoting

hemostasis can be vital in the hemorrhagic There is a constant balance in any given patient between hemostasis, thrombosis, and hemorrhage. Critical
patient and must be considered in lieu of/in illness, organ dysfunction, physiologic insults, and medications can all tip this balance in one direction or
the other. Knowing which variables to target and prioritize can help achieve hemostasis in the coagulopathic
addition to blood product transfusion. patient. Venous thromboembolism and transfusion are discussed separately in this manual.

Physiology of Coagulation
Coagulation is a complex interplay of multiple variables, initially triggered by tissue injury (Figure 34.1).
Abnormalities in the coagulation cascade are commonly encountered in the ICU, and an understanding of the
complexity of the coagulation pathways is essential in proper management of the ICU patient.

Acquired Coagulopathies
A. Hypocoagulable States
1. Factor Deciencies
Hepatic dysfunction, vitamin K deciency, biliary obstruction, and other nutritional decits can lead to
various factor deciencies. For example, in the case of Vitamin K deciency, levels of factors II, VII, IX,
and X along with Protein C, Protein S, and Protein Z are reduced, as they are dependent on Vitamin K for
synthesis, causing an overall hypocoagulable state.
cryoprecipitate, and/or factor concentrates will result in a relative dilution of the
native coagulation proteins. Large-volume crystalloid/colloid resuscitation can
have the same result.

B. Hypercoagulable states
1. HIT
Heparin-induced thrombocytopenia is the abnormal thrombocytopenia that
results from administration of one of the various forms of heparin. The
underlying pathology of this disease is the formation of abnormal antibodies
in response to heparin that bind and activate platelets. This activation leads to
thrombosis and platelet consumption.
2. Hypercoagulability of Malignancy
Malignancy can result in a prothrombotic state through tumor cell secretion
of procoagulants and inammatory cytokines, physical interaction of tumor
cells and blood, disruption of the normal endothelial layer, acute phase reactant
production, and inammation from necrosis.
3. Pregnancy
Normal pregnancy is accompanied by increases in brinogen and thrombin
(promoting thrombosis) and increased plasminogen activator inhibitor levels
(impairing brinolysis). Pregnancy can also result in a pathological state of
HELLP (hemolysis, elevated liver enzymes, low platelets) that can cause
spontaneous hepatic hemorrhage and even maternal death.
4. Trauma
Major trauma induces a hypercoagulable state, which is thought to arise
from increased and persistently elevated levels of thrombin in addition to
dysregulation of its breakdown.
5. Sepsis
Sepsis causes a systemic response to infection that includes a robust
inammatory response. This inammatory response includes increased levels
of cytokines that can activate the coagulation cascade and increased levels of
Figure 34.1 The Coagulation Cascade. [] procoagulants such as thrombin.
6. Other
2. Consumptive Coagulopathies Hyperhomocysteinemia, TTP/HUS, nephrotic syndrome, and antiphospholipid
antibody syndrome are other important hypercoagulable states.
Disseminated Intravascular Coagulation (DIC) is a pathological activation of the
coagulation cascade that results in widespread thrombosis and subsequent depletion of
the various proteins necessary for normal coagulation. Thrombocytopenia, thrombin- Congenital coagulopathies
induced factor consumption, and plasmin generation thus result in a hypocoagulable A. Hypocoagulable States
state. 1. Hemophilia A
3. Platelet Dysfunction and Deciency Hemophilia A is a sex-linked recessive deciency of factor VIII that can have a wide
In addition to the myriad of pharmacological agents that affect platelet function (as range of severity that relate to factor VIII activity level. Mild hemophiliacs can use
discussed below) there are also many pathological states that can lead to platelet DDAVP to stimulate release of factor VIII while treatment of the hemorrhaging patient
function inhibition and/or thrombocytopenia. The most commonly encountered in involves replacement of factor VIII with traditional FFP/cryoprecipitate or with newer
the critically ill patient include hypothermia, uremia, acidosis, and extracorporeal factor VIII concentrates. In cases of severe hemorrhage or for patients with factor VIII
circulation (such as hemodialysis, cardio-pulmonary bypass, ECMO, or ventricular inhibitors, NovoSeven can be used as an alternative (discussed below).
assist devices. 2. Hemophilia B
4. Hemodilution Hemophilia B is a sex-linked recessive deciency of factor IX that has a similar
In the patient requiring massive transfusion, transfusion of packed red blood cells clinical presentation to hemophilia A. Replacement of factor IX with concentrates is
without the appropriate additional transfusion of fresh frozen plasma, platelets, the indicated treatment in this patient population.

3. vWD antithrombin to exert its anticoagulant effect. The elimination half-life is 17-21 hours.
Von Willebrand Disease is the most common hereditary coagulopathy (but can also Although no evidence-based recommendations exist, a conservative management
be acquired) that results from a qualitative and/or quantitative deciency of von strategy is to delay elective surgery for 5 half-lives, or 4 days. Dose adjustment is
Willebrand factor (vWF). A bleeding tendency results that is more prominent in required for patients with renal insufciency.
tissues having high blood ow shear stress, where vWF is most active.
4. Other Rare Disorders D. Direct thrombin inhibitors
The various dysbrinogenemias, factor XIII deciency, the rare factor deciencies (V, The direct thrombin inhibitors (DTI) include dabigatran, lepirudin, argatroban, and
VII, X, XI), and prothrombin deciency (Factor II) are also important considerations bivalirudin. They interact with free or clot bound thrombin to inhibit the conversion
in the differential diagnosis of the coagulopathic patient. of brinogen to brin. The half-lives of the drugs vary. Conservative management
strategies suggest that patients on intravenous infusions of DTIs should have the drug
discontinued ve elimination half-lives before elective surgery or neuraxial blockade.
B. Hypercoagulable States There is no reversal agent for DTI related bleeding. DTIs are useful to prevent and
1. Factor V Leiden treat thrombotic events related to heparin induced thrombocytope